However, the following phase III studies revealed that high IFN signatures did not always explain more favorable response to type I IFN inhibitors [26, 27]. Clinical trials of other biologics such as rituximab, an anti-CD20 monoclonal antibody, and abatacept, a cytotoxic T lymphocyte-associated antigen 4 (CTLA4)–immunoglobulin fusion protein, failed to achieve the primary endpoints in SLE or LN patients [28–31]. The gene discussed is CTLA4; the disease is systemic lupus erythematosus.