We found that deep deletion of METTL3 was most prominent in undifferentiated stomach adenocarcinomas, whereas its amplification was dominant in cervical adenocarcinomas, ESCA, ovarian epithelial tumor, HNSC, non-small cell lung cancer, diffuse glioma, SARC, esophagogastric adenocarcinoma, invasive breast carcinoma, ACC, pheochromocytoma, and LIHC (Figure 1C). This evidence concerns the gene METTL3 and gastroesophageal junction adenocarcinoma.