Three potential explanations for this result are that (i) SPHK1 is more highly expressed and/or more bioactive in CD4 T cells than SPHK2, (ii) inhibition of SPHK1, but not SPHK2, promotes changes to the biochemical environment that reduce permissiveness to HIV-1 infection, and/or (iii) SPHK2 is not effectively targeted by ABC29460 to reduce susceptibility to infection at concentrations of this compound that maintain viability in primary CD4 T cells. Here, SPHK1 is linked to HIV-1 infection.