In addition to the recent evidence that miR-16 exerts its tumor suppressor role by targeting KRAS in colorectal cancer [47], we demonstrated that miR-16 directly targets the MAPK pathway at several levels and that the silencing operated by it on MAPK3 and MAP2K1 (Figure 8) restores its sensitivity to erlotinib in KRAS-mutated NSCLC both in vitro and in vivo. This evidence concerns the gene KRAS and neoplasm.