Using well-established models of bacteria-induced colon cancer and antibody-based cell depletion and cytokine neutralization protocols, the authors concluded that IL-17 and IL-22 produced by colonic ILC3 contribute to inflammation and tumor development, with an additional role for IL-22 to perpetuate the cancerous state by inducing proliferation of epithelial cells in a STAT-3-mediated mechanism [70]. This evidence concerns the gene IL17A and colonic neoplasm.