Step 1: Start from the protein named in the stem. ABCC2, the transporter also known as MRP2 or cMOAT, lives on the canalicular (bile-facing) membrane of the liver cell and is the main exporter of conjugated bilirubin into bile.
Step 2: Ask which hereditary jaundice arises when this exporter fails. When ABCC2 is mutated, conjugated bilirubin builds up inside the hepatocyte and spills back into blood, giving a direct hyperbilirubinemia and a melanin-like black liver on gross examination. That clinical picture defines Dubin-Johnson syndrome.
Step 3: Eliminate by mechanism. Rotor syndrome involves impaired hepatic storage rather than the canalicular pump. Crigler-Najjar and Gilbert syndromes both stem from reduced bilirubin conjugation through UGT1A1, so their problem sits upstream of MRP2 and produces indirect bilirubin.
Step 4: Only one option matches an MRP2/ABCC2 transport defect.
\[\boxed{\text{Dubin-Johnson syndrome}}\]