While the inherent genetic heterogeneity across the tested primary pancreatic cancer cell lines opens alternate explanations for any observed drug-phenotype correlations, we hypothesized that receptor tyrosine kinase-independent, genetically driven alternate activation of the MAPK pathway, like through mutant PLXNA1 signaling associated with elevated pErk levels (Fig 9D), might display a distinct drug phenotype. The gene discussed is PLXNA1; the disease is pancreatic neoplasm.