Likewise, Grp78 haploinsufficiency suppressed mutant Kras-driven lung tumorigenesis at least in part through activation of UPR induced cell death (50), and targeting GRP78 suppressed KRAS protein expression but not SRC proto-oncogene, nonreceptor tyrosine-protein kinase (SRC), or p85 and reduced viability of cancer cells bearing various KRAS mutations in lung, colon, and pancreatic cancer (51). The gene discussed is KRAS; the disease is familial pancreatic carcinoma.