In addition, JAK/STAT signaling has been shown to promote and modulate inflammatory processes [62], [63] leading to human BBB dysfunction in HIV infection [64], the latter dysfunction was mediated through CCR5 receptor which is involved in HIV-1 binding to HBVEC and activating the phosphoinositide-dependent kinase-1 (PDK1) and the serine-threonine protein kinase AKT [64]. This evidence concerns the gene SOAT1 and HIV infectious disease.