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. Here, U2AF1 is linked to cancer.