SLCO1A2 encodes organic anion-transporting polypeptide 1A2 (OATP1A2), a sodium-independent transporter mediating cellular uptake of diverse organic anions at the plasma membrane. The transporter handles endogenous substrates including bile acids (cholate, deoxycholate, and their conjugates), steroid sulfates (dehydroepiandrosterone 3-sulfate and estrone 3-sulfate), thyroid hormones, and retinol, with the latter being essential for maintaining the visual cycle. OATP1A2 also mediates uptake of clinically used drugs including methotrexate and paclitaxel, operating through a pH-sensitive mechanism with bicarbonate as the probable counteranion. SLCO1A2 expression is regulated by the vitamin D receptor and suppressed by inflammatory signaling through nuclear factor-κB. Genetic variation in SLCO1A2 has direct clinical relevance: loss-of-function variants (E184K, D185N, T259P, D288N) reduce membrane expression and transport capacity, and in rheumatoid arthritis patients, the 550AA genotype is associated with high risk of methotrexate-related adverse effects 1. Carriers of impaired SLCO1A2 variants may experience altered drug efficacy or enhanced toxicity 2. Beyond pharmacogenetics, SLCO1A2 variants show genome-wide significant associations with normal pressure hydrocephalus and progressive supranuclear palsy, likely reflecting roles in blood-brain and blood-cerebrospinal fluid barrier function 345. The transporter also influences treatment response to antimalarial drugs in Plasmodium vivax malaria 6.