Thus, our in vitro experiments with exogenous IFN-α and IFN-β suggest that the increase in S1PR1 that we observed on thymocytes during HIV infection may be more related to endogenous IFN-β than IFN-α and may be mediated to a greater extent by IFNAR2 than IFNAR1. The gene discussed is IFNAR1; the disease is HIV infectious disease.