In light of our present study suggesting tumor-suppressive role of Src in the context of oncogenic KRAS as well as recent reports demonstrating clinical utility of SHP2 inhibitors in the management of mutant KRAS-driven cancers7–11, inclusion of KRAS mutational status would be prudent for future clinical trials of Src and SHP2 inhibitors as mono or combination therapies. This evidence concerns the gene KRAS and neoplasm.