Thus, although EGFR and KRAS-mutant NSCLC represent in clinical scenarios two different subtypes, their pathways are biologically connected: co-targeting of EGFR receptor and downstream mediators belonging to RAS/MEK signaling has shown promising efficacy in pre-clinical and clinical studies in EGFR-mutant tumors [8,26], and resistance mechanisms to EGFR/KRAS targeting may overlap. This evidence concerns the gene KRAS and non-small cell lung carcinoma.