Hayashi et al. further illustrated that lysine methyltransferase 2C (KMT2C), AT-rich interaction domain 1A (ARID1A), GATA binding protein 6 (GATA6), TP53, SMAD4, KRAS proto-oncogene, and GTPase (KRAS) are all involved in pancreatic cancer formation [44], while Kawakubo et al. revealed that the epigenetic regulation of pancreatic cancer could affect its response to immunotherapy, including the combined applications of inhibitors against DNMT, HDAC, BET, and EZH2 [45]. This evidence concerns the gene SMAD4 and familial pancreatic carcinoma.