Loss of these functions, as observed in MYO6-deficient Snell’s waltzer mice and in humans with mutations in the MYO6 gene, contributes to various disease phenotypes, including deafness, astrogliosis, proteinuria, and hypertrophic cardiomyopathy (Avraham et al., 1995; Avraham et al., 1997; Melchionda et al., 2001; Mohiddin et al., 2004; Arden et al., 2016). Here, MYO6 is linked to hypertrophic cardiomyopathy.