However, administering IL‐2 restored antigen‐specific T‐cell responses and protective efficacy.[80] Our collective findings, including the reductions in M.tb burden, observed in RAG1‐KO studies[44] and the decreased T cell exhaustion seen in TCR‐KO studies (OM‐TB‐TKO group), align with these observations. The gene discussed is IL2; the disease is tuberculosis.