Overexpression of 90 K in 293 T cells reduced HIV-1 infection, while endogenous knockdown of 90 K in HeLa cells and primary macrophages enhanced HIV-1 infection; IFN-α stimulation upregulated cellular 90 K expression in 293 T cells and macrophages and enhanced its anti-HIV-1 infection activity [9]. The gene discussed is LGALS3BP; the disease is HIV-1 infection.