Ip et al. has recently shown that macrophages from the intestinal lamina propria of IL-10-null mice and from IL-10 receptor-deficient IBD patients with colitis accumulated mitochondria with higher ROS levels, aberrantly secreted IL-1β, and demonstrated increased mTORC1 and inflammasome activation, all of which strongly contributed to intestinal inflammation.13 Mice with colitis treated with antioxidants or rapamycin, an mTOR inhibitor, showed suppressed IL-1β secretion. This evidence concerns the gene IL1B and inflammatory bowel disease.