Mice deficient for Itch developed spontaneous colitis at 6–8 months of age associated with increased IL-17 levels in mucosal tissues and also exhibited higher tumor burden and increased incidence of colonic inflammation-associated cancer [57], indicating that Itch-modulated and RORγt-based ubiquitination can regulate IL-17-mediated colonic inflammation-associated cancer. The gene discussed is ITCH; the disease is cancer.