The disparate effects that CD4+ T cells may have on host immune protection, exemplified by the opposing outcomes of Th17 and Th1 effector responses on gonococcal infection discussed above, makes it somewhat foolhardy to try and difficult to extrapolate from cell-based in vitro studies to predict the global outcome of infection in vivo, particularly considering the central role that these cells play as both a cellular HIV target and drivers of host immunity against HIV infection. The gene discussed is CD4; the disease is infection.