To test how Smarcd3 contributes to early pancreas cancer establishment, we crossed a conditional Smarcd3f/f line35 to the KrasLSL/+; Ptf1a-Cre (KC) model, where embryonic activation of KRAS in pancreatic precursors drives the formation of benign PanIN lesions23, as well as the KrasLSL/+; Ptf1a-CreER and KrasLSL/+; Sox9-CreER36 models, where benign lesions are initiated in adult acinar or ductal cells respectively. This evidence concerns the gene SMARCD3 and pancreatic neoplasm.