To explore systematically the apparent antagonism between KRAS and MYC pathways and understand how cytotoxic drugs alter MYC expression and cancer cell viability, we measured their effects in isogenic NSCLC cell lines with stable expression of exogenous KRAS mutants (G12C, G12D and G12V) as well as upstream (EGFR) and downstream (PIK3CA, BRAF, CRAF, RALA) components of the RAS pathway (Figure 6A). The gene discussed is KRAS; the disease is non-small cell lung carcinoma.