Although the mechanisms underlying the beneficial effect of rhIL-2 immunotherapy remained uncompletely understood, our previous work indicated that the responses of the Th1 and Th2 subsets in patients with MDR-TB are more substantially suppressed13, while Th17 subset response seemed more preferentially enhanced15, as it was reported that CD4+ T cells fail to produce IL-2 during chronic TB infections11. The gene discussed is CD4; the disease is multidrug-resistant tuberculosis.