The results of these studies are controversial, since some authors suggested that cells from EC were resistant to infection because of selective up-regulation of cyclin-dependent kinase inhibitor p21 (Chen et al., 2011), whereas others reported resistance of EC CD4+ T cells to HIV-1 infection but showed that p21 plays no or indirect role in this phenomenon (Saez-Cirion et al., 2011). This evidence concerns the gene CD4 and HIV-1 infection.