KRAS and pancreatic ductal adenocarcinoma: However, recent data provide evidence that this independence may not be definite: (i) in KRAS mutant NSCLC cell lines, activation of PI3K depends on basal activity of wildtype IGF1R, illustrating a model for how oncogenic and normal signal transduction coordinate [136]; (ii) development of KRASG12D-driven pancreatic ductal adenocarcinoma is suppressed in the absence of EGFR [137,138]; and (iii) induced expression of ERBB2 and ERBB3 provokes resistance to MEK inhibition in KRAS+ lung and colorectal cell lines [139].