Furthermore, in lupus-susceptible mice, blocking of Rab geranylgeranyl transferase with Rab geranylgeranyl transferase inhibitor (3-PEHPC) could reverse dynamin-related protein 1 (Drp1) consumption, mitochondrial accumulation, and nephritis, confirming that HRES-1/Rab4 regulation of mitochondrial homeostasis is the pathogenesis and potential therapeutic target of SLE (323). The gene discussed is RAB4A; the disease is nephritis.