Mechanistically, the lung microbiota dysbiosis in this model, characterized by over-representation of various bacterial taxa like Herbaspirillum and Sphingomonadaceae, induced the production of interleukin-23 (IL-23) and interleukin-1β (IL-1β) from myeloid cells in a myeloid differentiation primary response 88 (MYD88)-dependent manner, leading in turn to lung-resident γδ T cell proliferation and expression of IL-17 and other pro-inflammatory factors to up-regulate local inflammation and eventually tumor cell proliferation. The gene discussed is IL37; the disease is neoplasm.