It has been shown that in CRC cell lines mutated KRAS can activate downstream effectors of the PI3K pathway, such as Ras homolog gene family member A (RhoA), Ras-related C3 botulinum toxin substrate 1 (Rac1), and cell division cycle 42 (Cdc42), and in synergy with TGF-β signaling can promote EMT inducing a decrease of E-cadherin expression and an increase of vimentin expression (Figure 3) (40, 77, 78). This evidence concerns the gene KRAS and colorectal carcinoma.