Additionally, the transgenic overexpression of PGC-1α or treatment with drugs (NAD+ precursor Nicotinamide (NAM), AMPK, and Phosphodiesterase inhibitors and anti-TWEAK antibodies) that preserve PGC-1α expression resulted in increased mitochondrial mass and reduced kidney injury in experimental AKI [34,45], suggesting that therapeutic approaches that promote PGC-1α expression and/or mitochondrial mass may be beneficial in AKI. This evidence concerns the gene TNFSF12 and acute kidney injury.