Moreover, it induces an increase in the activation of the intestinal dendritic cells (DCs), which leads to an amplified expression and release of pro-inflammatory molecules such as tumor necrosis factor-alpha (TNF-α) associated with IBD [10, 11]. LRRK2 inhibitors decreased Dectin-1-induced TNF-α production by mouse DCs and ameliorated colitis, both in control and LRRK2 transgenic animals [10]. This evidence concerns the gene LRRK2 and inflammatory bowel disease.