UNC45A and microvillus inclusion disease: Strikingly, treatment of UNC45KO Caco-2 cells with the proteasome inhibitor MG132 resulted in the appearance of large myosin VB–positive aggregates (Figure 4B), indicating that UNC45A is critical for preventing aggregation and incorrect folding of myosin VB, which overall suggests that UNC45A deficiency could phenocopy the MVID phenotype.