Therefore, according to the different immune endotypes in TB patients, IL-17A was unable to augment autophagy in non-responder patients because of a defect in the MAPK1/3 signaling pathway, whereas both IFN-γ and IL-17A increased autophagy levels in patients with a strong immunity to Mtb, promoting mycobacterial killing [31]. This evidence concerns the gene IL17A and tuberculosis.