“…KRAS mutations usually target a ''hot spot'' at codon 12, but they may also affect codons 13 and 61 [4-6, 29, 30]. Akin to other proteins of the Ras family, KRAS encodes a GTPase that works as an activation/ ACC acinar cell carcinoma, BRAF v-Raf murine sarcoma viral oncogene homolog B, IPMN intraductal papillary mucinous neoplasm, Jak1 janus kinase 1, LOH loss of heterozygosity, MCN mucinous cystic neoplasm, MEK mitogen-activated protein/extracellular-signal-regulated kinase kinase, mTOR mechanistic target of rapamycin, PanNET pancreatic neuroendocrine tumor, PARP poly(ADP-ribose) polymerase, PB pancreatoblastoma, PDA pancreatic ductal adenocarcinoma, SCA serous cystadenoma, SPN solid-pseudopapillary neoplasm inactivation switch that controls a number of downstream pathways that affect proliferation, differentiation, and cell survival [31][32][33][34]. A third of PDAs without a KRAS mutation harbor BRAF mutations, highlighting the importance of Ras signaling for PDA formation [35].…”