In colorectal cancer, constitutively activated mutant KRAS or altered stimulation of pathway components (mainly RAS, RAF, MEK) results in the hyperactivation of the mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase 1 and 2 (ERK1/2) and positively modulates tumor proliferation by increasing GLI1 transcriptional activity and expression of Hh target genes (54, 70, 71). This evidence concerns the gene MAPK3 and colorectal cancer.