UROD (uroporphyrinogen decarboxylase) is a cytosolic enzyme catalyzing the sequential decarboxylation of uroporphyrinogen's acetate side chains to form coproporphyrinogen, representing the fifth step in heme biosynthesis 1. Only coproporphyrinogen III can ultimately be converted to heme, though both uroporphyrinogen isomers I and III may serve as substrates 1. UROD deficiency causes porphyria cutanea tarda (PCT), the most common human porphyria worldwide 2. Two forms exist: type I (sporadic, ~80% of cases) involves acquired hepatic UROD deficiency, while type II (familial) results from autosomal dominant UROD mutations with low penetrance 3. PCT manifests as skin fragility, blistering lesions on sun-exposed areas, and elevated porphyrins 4. Critically, hepatic iron overload is central to pathogenesis—UROD is inactivated through an iron-dependent process targeting its catalytic site, and iron depletion produces remission while iron replenishment causes relapse 3. Multiple factors precipitate PCT, including alcohol abuse, hepatitis C infection, HIV, estrogen use, and UROD mutations 5. Clinical management involves therapeutic phlebotomy for iron depletion and low-dose hydroxychloroquine to reduce hepatic porphyrin content, both equally effective treatments 5.