In the pathological environment of intestinal malignant tumors, the original calcium homeostasis is broken, forming a “new homeostasis” in which the [Ca2+]i of colorectal glandular epithelial tumors is increased, and the increase in [Ca2+]i activates calmodulin kinase II (CaMKII) and hypoxia-inducible factor-1a (HIF1a), which are involved in tumor progression [26, 27]. The gene discussed is CAMK2G; the disease is neoplasm.