In a recent study by Sato et al,35 a link is shown between hyperglycemia, the activation of MYC through STAT3, and the development of pancreatic cancer.36 Similarly, estrogen receptor-related pathways have been linked to an increased risk of developing pancreatic cancer.37–39 Alternatively, the activation of c-MYC and estrogen response genes could be a compensatory response to the reduced acinar volume19 to initiate proliferation of the tissue. This evidence concerns the gene MYC and familial pancreatic carcinoma.