Recent integrated multi-platform sequencing analyses of pancreatic cancer ductal adenocarcinoma (PDAC) have revealed ARID1A mutations in ~6% of cases [2], besides predominant somatic mutations of KRAS, TP53, SMAD4 and CDKN2A. These predicted loss-of-function alterations has led to the prevailing assumption that ARID1A behaves as a classic tumor suppressor gene (TSG), likely demonstrating genetic cooperation with mutant KRAS in pancreatic tumorigenesis. This evidence concerns the gene ARID1A and familial pancreatic carcinoma.