These studies indicate a strong correlation between low levels of intracellular dNTPs and restriction of HIV-1 infection; however, addition of deoxynucleotides into resting CD4+ T-cells or macrophages to increase the intracellular dNTP pool cannot fully restore HIV-1 or SIV infections [24, 64], suggesting that decreasing the intracellular dNTP pool by SAMHD1 may not be the sole mechanism underlying retroviral restriction in nondividing cells (Figure 2). The gene discussed is SAMHD1; the disease is HIV-1 infection.