It has been found that in patients with colorectal cancer, CCAT1 can modulate MLCK in a miR-185-3p-dependent manner, regulate the role of tight junction proteins including claudin and ZO-1 in the distribution of MLCK, increase intestinal epithelial TJ permeability, and promote the malignant change of IBD [43]. The gene discussed is MYLK; the disease is inflammatory bowel disease.