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. The gene discussed is PTPN11; the disease is neoplasm.