Indeed, Tran et al. performed microarray sequencing of kidney-derived RNA from mice at baseline and after lipopolysaccharide (LPS) administration (a modeling method for SA-AKI) and found that genes involved in oxidative phosphorylation, including the mitochondrial biogenesis regulator PGC-1α, are suppressed during SA-AKI and reactivated following the recovery of renal function, indicating that mitochondrial dysfunction is a major contributor to SA-AKI (Tran et al., 2011). The gene discussed is PPARGC1A; the disease is acute kidney injury.