In tuberculosis, which enhances lung cancer risk (Ho et al., 2021), Mycobacterium bovis Bacille–Calmette–Guerín (BCG) infection upregulated PD-L1, CD40, and CD69 via induced expression of TLR2 and TLR4 in both M-MDSCs and PMN-MDSCs in mice, also upregulating iNOS expression, leading to an increased NO production necessary for the suppression of T-cells in BCG-infected mice (John et al., 2019). This evidence concerns the gene CD69 and tuberculosis.