It functions as a tumor suppressor involved in multiple solid tumors with distinct mechanisms, including colorectal adenocarcinoma, kidney renal clear cell carcinoma, prostate cancer, and pancreatic ductal adenocarcinoma (PDAC).[8] Therefore, it is of great significance to develop patient‐tailored therapies based on SETD2‐H3K36me3 mutations or deficiency. Here, SETD2 is linked to neoplasm.