RBBP9 and neoplasm: By mediating IL6/STAT3 activation, mTORC signaling promotes a regenerative process after injury in the intestines33; moreover, strong evidence links mTORC1 hyperactivation with UC and CAC.34, 35, 36 These findings support the concept that the increased activity of both mTORC1 and IL6/JAK/STAT3 signaling enhances tumor formation in an inflammation-dependent AOM/DSS model in RBBP9-deficient mice.