CROT (carnitine O-octanoyltransferase) is a peroxisomal enzyme that catalyzes beta-oxidation of medium-chain fatty acids (C6-C10), with particular activity in converting 4,8-dimethylnonanoyl-CoA during pristanic acid metabolism [UniProt]. The enzyme facilitates fatty acid oxidation and energy generation while regulating lipid homeostasis in skeletal muscle and other tissues 1. Clinically, CROT expression is dysregulated in multiple cancers with significant functional consequences. In non-small cell lung cancer, CROT overexpression drives chemoresistance by enhancing peroxisomal fatty acid oxidation, stabilizing Nrf2 transcription factor via ROS-mediated mechanisms, and inhibiting ferroptosis—a key chemotherapy-induced cell death pathway 2. Conversely, CROT is downregulated in ovarian cancer, where loss of expression promotes cell proliferation, migration, and paclitaxel resistance through TGF-β signaling pathway activation; the miR-33a-5p/CROT axis regulates these processes 3. In prostate cancer, low FECH/CROT expression following androgen deprivation therapy predicts recurrence, indicating androgen-regulated metabolic reprogramming 4. Beyond cancer, CROT dysregulation associates with hypertension and stroke pathogenesis through altered fatty acid metabolism and inflammatory responses 5, while upregulation occurs in idiopathic pulmonary fibrosis where CROT silencing reduces epithelial-mesenchymal transition 6. These findings identify CROT as a metabolic regulator with therapeutic potential in cancer and pulmonary disease.