In addition, endogenous estrogen (E) interacts with IGF-I/IR traits and their signaling pathways as well as their target genes through a synergistic cross-talk mechanism, leading to an enhanced anabolic state necessary for tumor growth.[24–28] In postmenopausal women, endogenous E level is associated with higher risk of CRC.[4] Exogenous E has a different effect than endogenous E on CRC risk. The gene discussed is INSR; the disease is colorectal carcinoma.