On the other hand, the effect of conditional Irf5 ablation after disease onset in Lyn–/– mice on the aberrant TMRM signals in Ly6C− monocytes and pDCs appeared to be limited (Supplementary Fig. 8e), implying that IRF5 may be involved in a process causing abnormal mitochondrial activity at an early stage of SLE pathogenesis. The gene discussed is IRF5; the disease is systemic lupus erythematosus.