ALDH1B1 is a mitochondrial NAD(P)+-dependent oxidoreductase that catalyzes the oxidation of aldehydes to carboxylic acids 1. Its primary function involves detoxifying lipid peroxidation by-products and metabolizing diverse aldehyde substrates, including acetaldehyde, 4-hydroxynonenal, nitroglycerin, and all-trans retinaldehyde 23. ALDH1B1 also participates in retinoic acid metabolism through retinaldehyde oxidation 4. Mechanistically, ALDH1B1 modulates reactive oxygen species (ROS) levels in cells; NR5A2 transcriptionally regulates ALDH1B1 to maintain ROS homeostasis and prevent pyroptosis 5. In cancer contexts, ALDH1B1 overexpression promotes epithelial-mesenchymal transition, chemoresistance, and cancer stem cell phenotypes through activation of Wnt, Notch, Hippo, and TGF-β signaling pathways 2. Clinically, ALDH1B1 expression correlates with poor prognosis across multiple cancer types including lung adenocarcinoma, colorectal cancer, nasopharyngeal carcinoma, and diffuse large B-cell lymphoma 2678. ALDH1B1 inhibitors selectively suppress cancer cell growth and potentiate chemotherapy responses 68. Additionally, reduced ALDH1B1 expression in Alzheimer's disease astrocytes impairs axon initial segment integrity through compromised retinoic acid synthesis 4. Human ALDH1B1 polymorphisms (A86V, L107R, M253V) variably affect catalytic activity and substrate metabolism 3.