Because mutations of myosin-Va or Rab27a had been known to cause similar melanosome transport defects in dilute and ashen mice and in human Griscelli syndrome type 1 and type 2 patients, respectively (Ménasche et al., 2000; Mercer et al., 1991; Pastural et al., 1997; Wilson et al., 2000), the direct interactions of melanophilin with myosin-Va and Rab27a were soon discovered to retain melanosomes within the actin networks in the cell periphery (Fukuda et al., 2002a; Nagashima et al., 2002; Strom et al., 2002; Wu et al., 2002). This evidence concerns the gene MYO5A and Griscelli disease type 1.