Although FAM83A has previously been reported to have an important role in therapeutic resistance to tyrosine kinase inhibitors in breast cancer, numerous studies have demonstrated oncogenic K-RAS mutations are the major mechanism of epidermal growth factor receptor-mediated resistance in pancreatic cancer;33, 34 approximately 90% of patients with pancreatic cancer harbor gain-of-function K-RAS mutation.35 Therefore, FAM83A-induced pancreatic progression may be mediated via other mechanisms. Here, SACK1A is linked to familial pancreatic carcinoma.