Taken together, we propose that upon HIV-1 infection in T cells, the retroviral Gag reaches the cell plasma membrane for assembling in already-existing area less dense in cortical F-actin and that thereafter Gag could recruit the host cell factor Arpin is fostering this process since decrease in actin branching favors HIV-1 Gag assembling. Here, ARPIN is linked to HIV-1 infection.