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). This evidence concerns the gene SRC and familial pancreatic carcinoma.