Based on these observations, we proposed a possible mechanistic circuit of the cytoprotective effect exerted by HIV-1 infection and intracellular Tat protein (Figure 4A): the decrease in PTEN levels observed during HIV-1 infection and Tat expression may result from the possible destabilization of p53, caused by the direct binding of intracellular Tat to p53. The gene discussed is TP53; the disease is HIV-1 infection.