In a pancreatic cancer model, Qiu et al. found that 2-AG suppresses tumor proliferation via activation of the CB1 receptor, rather than the CB2 receptor, and fosters the maturation of DC phenotypes and production of pro-inflammatory cytokines through up-regulation of the signal transducer and activator of transcription 6 (p-STAT6) [18]. This evidence concerns the gene STAT6 and familial pancreatic carcinoma.