Nonetheless, a decrease in BCA2 was observed for both vector-treated cells and cells overexpressing HA-BCA2 infected with HIV-1, suggesting that either the activation of additional innate signaling cascades in response to HIV-1 infection leads to a reduction in BCA2 or HIV-1 partially circumvents this barrier by decreasing the steady-state levels of the protein. The gene discussed is RNF115; the disease is HIV-1 infection.