These data are confirmatory of earlier work in the lab revealing that genotype alone was not enough to account for elevated IRF5 expression in primary immune cells of SLE patients and enhanced IRF5 alternative splicing was, at least in part, due to elevated levels of spliceosome components in SLE patients as overexpression of many of these factors led to increased IRF5 alternative splicing [15]. The gene discussed is IRF5; the disease is systemic lupus erythematosus.