Step 1: The question links the canalicular transporter protein MRP2 to a specific inherited hyperbilirubinemia. MRP2 is also called the canalicular multispecific organic anion transporter (cMOAT) or ABCC2, and it pumps conjugated bilirubin from the hepatocyte into bile.
Step 2: Dubin-Johnson syndrome is an autosomal recessive disorder caused by a mutation in the gene that codes for this MRP2/ABCC2 protein. Loss of the transporter blocks excretion of conjugated bilirubin, producing a conjugated (direct) hyperbilirubinemia with a characteristic black pigmented liver.
Step 3: The distractors point to different defects. Rotor syndrome is a defect of hepatic storage and uptake with a non-pigmented liver. Crigler-Najjar and Gilbert syndromes are defects of UGT1A1 (glucuronosyl transferase), so they cause unconjugated hyperbilirubinemia, not an MRP2 problem.
Step 4: Because only Dubin-Johnson syndrome is caused by an MRP2/ABCC2 mutation, option b is correct.