As SAMHD1 limits HIV-1 cDNA synthesis in myeloid cells (14, 54), it was hypothesized that degradation of SAMHD1 by Vpx in DCs would result in productive HIV-1 infection and the synthesis of viral proteins that would directly enter antigen presentation, thereby strengthening the T-cell response to infection (94). The gene discussed is SAMHD1; the disease is HIV-1 infection.