The bilateral labia minora lesions were resected general anesthesia on August 29, 2016. The operation was successful, and intraoperative blood loss was about 10 ml. After 40 months of postoperative follow-up, no recurrence or appearance of other tumors were noted. We recommend surgical removal of lesions in the genital area during adolescence or before adulthood. Adolescence may be the best period for surgical intervention owing to a greater risk of malignant change in adulthood. On the other hand, surgical risk should be avoided in children considering the low incidence of malignant transformation. We recommend surgical removal of lesions in the genital area during adolescence or before adulthood. Adolescence may be the best period for surgical intervention owing to a greater risk of malignant change in adulthood. On the other hand, surgical risk should be avoided in children considering the low incidence of malignant transformation. Genotypic and histological evolution of non-small-cell lung cancer (NSCLC) into small-cell lung cancer (SCLC) has been described as a mechanism of acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy. However, the number of clinical cases is rare. Two lung adenocarcinoma patients with EGFR mutations who recurred after radical resection transformed into SCLC under treatment with the sequential first- and third-generation EGFR-TKIs. The 2 cases were both confirmed as SCLC by pathological rebiopsy after EGFR-TKIs resistance. Case 1 was treated with etoposide plus cisplatin (EP) regimen and erlotinib, while case 2 was treated with erlotinib and EP followed by oral etoposide. Case 1 treated with EP only achieved 3-month progression-free survival (PFS), which is the first case that reported T790 M/C797S cis-mutation for osimertinib resistance before the SCLC transformation. However, case 2 treated with erlotinib and EP followed by oral etoposide, PFS lasted for 8 months. The cases highlighted the importance of rebiopsy that identified pathologically SCLC transformation after EGFR-TKI resistance, and suggested the treatment of erlotinib plus EP followed by etoposide, which could provide a reference for such phenotype. The cases highlighted the importance of rebiopsy that identified pathologically SCLC transformation after EGFR-TKI resistance, and suggested the treatment of erlotinib plus EP followed by etoposide, which could provide a reference for such phenotype. Poststroke dyskinesia is the most common clinical symptom after stroke, which greatly affects the patients' daily life. Eye-acupuncture is an effective method for stroke. And the rehabilitation training has been widely used for patients suffer from stroke. However, whether eye-acupuncture combined with rehabilitation training has greater clinical efficacy for poststroke dyskinesia is still unknown. Our aim in this systematic review was to evaluate the clinical efficacy of eye-acupuncture combined with rehabilitation training (EACRT) as a treatment for dyskinesia after stroke. We will search the following 4 databases of registered trials and 7 electronic databases from inception to March 2021Cochrane Stroke Group, Cochrane Central Register of Controlled, the World Health Organization International Clinical Trials Registry Platform, the Chinese Clinical Trial Registry; PubMed, MEDLINE, Embase, CNKI, VIP, WanFang, and CBM. All relevant randomized controlled trials focus on EACRT will be included. The primary outcome will be the Fugl-Meyer Assessment. The Secondary outcomes will include Activity of Daily Living, clinical effective rate and the Visual Analogue Score. Two reviewers will independently conduct the Study selection and data extraction. The data synthesis and assessment of risk of bias will be performed by RevMan5.2. The ethical approval is unnecessary that systematic review is based on published articles other than patients. The results of this meta-analysis will be published in an open access (OA) journal according to the Preferred Reporting Item for Systematic Review and Meta-analysis (PRISMA). CRD42020168278. CRD42020168278. Adrenocortical carcinoma (ACC) is considered a rare cancer with poor prognosis. We used public datasets from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases to assess the relationships between N6-methyladenosine (m6A)-related genes and ACC.We used the Wilcoxon signed-rank test to compare m6A-related gene expression in ACC tissues with that in normal tissues. Then, ACC patients were grouped based on a cluster analysis of m6A-related gene expression. m6A-related genes that were significantly associated with survival were incorporated into a risk signature, and 2 groups were divided according to median risk score. Fisher exact tests were utilized to analyze differences in clinical variables between groups. We compared the overall survival (OS) rates of the groups by means of Kaplan-Meier curves and Cox regression analyses.We found that RBM15, ZC3H3, YTDHF1, YTDHF2, and ALBH5 were overexpressed in ACC and that KIAA1429, YTHDC1, HNRNPC, WTAP, METTL3, and FTO were down regulated in with survival were incorporated into a risk signature, and 2 groups were divided according to median risk score. https://www.selleckchem.com/products/3-deazaneplanocin-a-dznep.html Fisher exact tests were utilized to analyze differences in clinical variables between groups. We compared the overall survival (OS) rates of the groups by means of Kaplan-Meier curves and Cox regression analyses.We found that RBM15, ZC3H3, YTDHF1, YTDHF2, and ALBH5 were overexpressed in ACC and that KIAA1429, YTHDC1, HNRNPC, WTAP, METTL3, and FTO were down regulated in ACC. In addition, membership in cluster 2 or the high-risk group was associated with advanced clinical factors and poor prognosis. The univariable and multivariable Cox regression analyses showed that risk score can be considered an independent prognostic factor for ACC.We found that the expression of m6A-related genes could be used as an independent prognostic factor in ACC. However, the current study has some limitations, and further studies of m6A-related genes in ACC are needed.