In particular, Jin et al. [17] proved that the microbiota can promote the secretion of γδT cells, further accelerating inflammation and tumour cell proliferation in lung cancer driven by the Kras mutation and the loss of p53. Interestingly, in the current study, we observed an obvious decrease in IFN-γ secretion by NK cells and CD8+T cells in the lungs of Kras mice with long-term microbiota depletion, suggesting that the main function of IFN-γ in the lung microenvironment may be to synergize/promote IL-17A-associated inflammation, thus promoting the development of lung cancer (Figure 3). The gene discussed is KRAS; the disease is neoplasm.