KRAS and cancer: The results suggested that siRNAs targeting RUVBL1, HSPA9, XPO1, and SLC38A2 resulted in the strongest decrease in cancer cell viability but not of normal fibroblasts (Supplementary Fig. 2D); thus, we concluded that the proteins encoded by these genes could lie at the intersection of vital programs of cancers driven by mutant TP53, mutant KRAS, and hyperactive MYC and could be tested as therapeutic targets.