Comparing the aPL frequencies within the HIV group, there were no statistically significant differences between the ACS+: HIV+ and ACS-: HIV+ groups but analysis of the actual aPL titres revealed higher levels of β2-GP-1 IgM as well as aPT (IgG, IgM, IgA) in the ACS-: HIV+ group possibly due to a greater degree of immunosuppresion and immune dysregulation [3], suggesting that the higher frequencies of aPL seen in HIV patients are an epiphenomenon of HIV infection rather than causally linked to thrombotic events. The gene discussed is CD79A; the disease is HIV infectious disease.