Lkb1 and Setd2 inactivation are two of the strongest drivers of KRAS mutant tumor growth; however, their inactivation reduced EGFR mutant tumor growth.8 These results correlate with the relative frequency of LKB1 and SETD2 alterations in human EGFR and KRAS mutant lung tumors, suggesting the existence of a synthetic lethal relationship between Lkb1/Setd2 inactivation and oncogenic EGFR. This evidence concerns the gene KRAS and neoplasm.