For example, loss of KMT2D in the early stage can collaborate with the upregulation of Bcl‐2 oncogene to facilitate lymphoma development.[52, 53] Lung‐specific KMT2D loss significantly promotes lung tumorigenesis and pro‐tumorigenic programming in mice, including glycolysis, supporting its role as a tumor suppressor.[54] In line with these studies, the function analysis in the present study uncovered that knockdown of KMT2D dramatically boosted the proliferation, migration, and invasion of PDAC cells. This evidence concerns the gene KMT2D and neoplasm.