This has been studied principally in CKD, where the downregulation of PGC-1α by transforming growth factor-beta (TGF-ß)/mothers against decapentaplegic homolog 1 (SMAD1) produces the diminish of PPARα abundance and, in consequence, the decrease of CPT1 (Gao and Chen 2022), which promotes apoptosis and fibrosis (Kang et al. 2015). The gene discussed is PPARGC1A; the disease is chronic kidney disease.