Human blood monocytes and resting CD4+ T-cells from SAMHD1-deficient AGS patients are more susceptible to in vitro HIV-1 infection compared with normal cells[3,5,6], suggesting that hSAMHD1 contributes to HIV-1 restriction in non-cycling immune cells through an intrinsic mechanism. This evidence concerns the gene SAMHD1 and Aicardi-Goutieres syndrome.