Jin et al. [79], using germ-free preclinical lung cancer models, demonstrated that the lung commensal microbiome can induce the activation and proliferation of γδ T cells by stimulating myeloid cells to produce Myd88-dependent IL-23, IL-1β, and IL-17, and lead to a pro-inflammatory state that induces tumor proliferation. This evidence concerns the gene IL17A and neoplasm.