Apoptosis induced by mitochondrial damage is the key molecular mechanism of AKI-CKD progression (Zhang et al. 2021), Yang et al. identified CD36 in purified mitochondria, and suppression of CD36 protein modifications through genetic or pharmacological methods could potentially protect against kidney fibrosis by switching fatty acids from an accumulation to a consumption phenotype (Yang et al. 2017). The gene discussed is CD36; the disease is acute kidney injury.