Nevertheless, as Usp22 deletion in vivo caused strong defects in various Ig isotypes but less so to IgA, Usp22 could be exploited as a therapeutic target in IgG or IgE-mediated autoimmune diseases, such as systemic lupus erythematosus, autoimmune thrombocytopenia, and asthma. The gene discussed is CD79A; the disease is systemic lupus erythematosus.