In lung and pancreatic cancer cells with mutated KRAS, treatment with trametinib, a MEK inhibitor which acts downstream of KRAS to suppress MAPK cascade, led to a compensatory response through activation of FGFR1 and subsequent phosphorylation of FRS2, thus resulting in alternative signal transduction and generating adaptive drug resistance [61]. The gene discussed is KRAS; the disease is familial pancreatic carcinoma.