2005), although subtle defects in stereocilia (Jagger et al. 2011), renal tubular cells (Li et al. 2007), and hypothalamic neurones (Heydet et al. 2013) have been described in murine models of Alström syndrome. It has been speculated that loss of ALMS1 leads to functional rather than anatomical defects in cilia, compromising, for example, vesicle transport from the Golgi apparatus to the cilium and/or intraflagellar transport (Hearn et al. 2005; Girard and Petrovsky 2011). This evidence concerns the gene ALMS1 and Alstrom syndrome.