Researches [26, 27] have shown that the overexpression of ErbB4 in intestinal mucosa of CD patients and CD mice may inhibit epithelial cell apoptosis induced by TNF-α and NF-κB and ameliorate colonic tissue damage. LRRK2 is involved in innate immune activities, and the loss of its function may cause a significant deficit in monocyte autophagy [28, 29], which is closely related to the onset of CD and colitis [30]. LRRK2 knock-out animals also demonstrate exacerbated colonic inflammation in an experimental model of colitis [31]. Here, ERBB4 is linked to inflammatory response.