Contextually, a Th2 shift in the tumor microenvironment, especially for CRC, strongly contributes to cancer relapse, metastasis, and worse prognosis (42, 43) although, according to existing contradictory evidence, excess inflammation caused by CD4+ and CD8+ IL-17-producing T cells or the immunosuppression induced by Tregs may lead to carcinogenesis (44, 45). The gene discussed is IL17A; the disease is neoplasm.