Notably, distinct mechanisms were shown to be involved in mediating the effects of PI3K p110α inhibition in the KRAS and KRAS/PIK3CA mutant CRC cells which could be explained, at least in part, by the coexistence of KRAS and PIK3CA mutations but also by other features including the type of KRAS mutation (HCT116, KRASG13D; SW480, KRASG12V). Here, KRAS is linked to colorectal carcinoma.