Since LRRK2 induces NFAT expression [38], and exacerbated NFAT-expression associated with IL-17A production has been observed in human and mouse colitis [39], [40], we suggest that the surge of IL-17A in Ncf1* mice may be the result of a poor regulation of LRRK2-activity in the absence of ROS, thus stressing LRRK2-role in colitis susceptibility. The gene discussed is IL17A; the disease is colitis.