Importantly, HIV infection itself has recently emerged as an independent contributor to cardiovascular disease in this population [2], [4]–[6], which may be at least partially explained by the activities of the HIV virion envelope protein gp120 and the transcription activator Tat in endothelial cells [7], [8], and the synergistic interactions of these with HIV-induced cytokines, such as TNF-α [9]. This evidence concerns the gene ITIH4 and cardiovascular disorder.