This study analyzed the processing and trafficking of melanogenic proteins in primary melanocytes from mice with the underwhite (uw) mutation, a model for oculocutaneous albinism (OCA) type 4 in humans. The researchers found that uw-mutant melanocytes constantly secrete dark vesicles containing tyrosinase and other melanogenic enzymes into the medium, unlike wild-type melanocytes. Although tyrosinase synthesis was similar between uw-mutant and wild-type cells, tyrosinase activity and melanosome enrichment were reduced in uw-mutant cells. The abnormal tyrosinase secretion from uw-mutant cells, along with other findings, suggests OCA4 disrup