BCL2L1 and pancreatic neuroendocrine tumor: Using two engineered Bcl‐xL mutants that cannot bind to Bax and Bak and therefore are defective in antiapoptotic function, we demonstrated that these engineered mutants as well as wild‐type (WT) Bcl‐xL are capable of inducing epithelial‐mesenchymal transition (EMT), migration, invasion, and stemness in both pancreatic neuroendocrine tumor and breast cancer cell lines.3, 4