IGF-1 activates proinflammatory signalling via mitogen-activated protein kinase (MAPK) (by binding to IGF-1R) and the phosphatidylinositol 3-kinase (PI3K)/serine-threonine kinase (AKT) pathway, both of which affect colorectal epithelial proliferation, differentiation, and apoptosis and contribute to the development of CRC (14). This evidence concerns the gene IGF1R and colorectal carcinoma.