The Beijing genotype is believed that it might confer a type of gene with more expressions, interacting with the host immune system harboring a variant of the Toll-interleukin 2 receptor (TLR2)[24, 25, 47], known to trigger a cytokine cascade upon recognition of MTB, increased TB susceptibility only in patients infected with a Beijing strain, releasing the immunologic substances, such as chemokine 10 (CK10), tumor necrosis factor α (TNF-α) [48], interferon γ (IFN-γ) and interleukin 17 (IL-17) [49]. This evidence concerns the gene IFNG and tuberculosis.