For instance, the plasma level of IL-6 is significantly elevated in patients with IBD, and the increased IL-6 activates STAT3/JAKl signaling, promoting cell proliferation, evolution, and tumorigenic progression [94]; inhibition of JAKl signaling or IL-6 deficiency by targeted disruption diminishes CRC incidence and progression [108, 109]. This evidence concerns the gene IL6 and colorectal carcinoma.