Additionally, a theory to explain the growth of neoplastic colon tumors has been proposed, according to which excessive levels of endocrine or autocrine GH, such as those caused by acromegaly or injury and inflammation of colonic DNA, inactivate genes involved in tumor suppression, inhibit apoptosis, and accelerate the epithelial-to-mesenchymal transition, resulting in alterations that promote malignancy in the intestinal mucosal field modification [41]. Here, GH1 is linked to colonic neoplasm.