SF3B1 and neoplasm: Dysregulation of AS is a hallmark of cancer, enabling tumor cells to evade apoptosis, enhance proliferation, and develop drug resistance.[9, 11, 27, 28] In EC, AS has been increasingly recognized as a key contributor to tumor progression; however, the specific mechanisms and functional consequences of these aberrant splicing events remain poorly defined.[29, 30] Several core splicing factors—such as SF3B1, SRSF2, and U2AF1—have been implicated in the pathogenesis of both hematologic and solid tumors by altering the splicing of critical oncogenes and tumor suppressors.