Firstly, the infection with HIV reduces phosphatase and tensin homolog (PTEN) levels.41 Prior oncology investigations revealed that constitutive PD-L1 expression due to PTEN loss might lead to resistance to other cancer immunotherapy approaches by actively suppressing antitumor T cells.42,43 Hence, we hypothesized that the lack of PD-L1 response may be due to the decrease in PTEN levels after HIV infection. The gene discussed is PTEN; the disease is HIV infectious disease.