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. This evidence concerns the gene CD79A and asthma.