Given the pleiotropic role of both oncogenic KRAS and SHP2 in modulating cancer-cell intrinsic mechanisms, including indirect regulation of the TME, and the cancer-cell extrinsic functions of SHP2, there are several potential mechanisms by which combined inhibition of KRASG12C and SHP2 could sensitise immune evasive tumours to anti-PD-1 therapies. Here, KRAS is linked to neoplasm.