RAB8A and microvillus inclusion disease: Mutagenesis of residues in myosin Vb that mediate this protein's interaction with either RAB11A or RAB8A, and the subsequent introduction of these mutant forms into myosin Vb-silenced human Caco-2 cells (Caucasian colon adenocarcinoma), revealed that the uncoupling of myosin Vb from both RAB11A and RAB8A forms the basis of MVID pathogenesis (Knowles et al., 2014).