Using the soluble form of the IL-2Rα (sIL-2Rα) as a surrogate marker of IL-2-mediated T cell activation, it was found that HIV infection is associated with low serum levels of sIL-2Rα in patients with TB, even when CD4+ lymphocyte counts are relatively well preserved, and that impaired IL-2 signaling could contribute to the profound impact that HIV has had on both the incidence and clinicopathological manifestations of TB [48]. The gene discussed is CD4; the disease is tuberculosis.