Consistent with the manifestations of IDDCA patients, phenotypic characterization of Gnb5 loss in mice and our zebrafish gnb5 knockout showed, respectively, abnormalities of neuronal development, including hyperactivity and an altered motor capacity, impaired ocular response, and cardiac sinus node dysfunction (Chen et al., 2003; Wang et al., 2011; Zhang et al., 2011; Xie et al., 2012; Lodder et al., 2016), corroborating the importance of GNB5 for neuronal signaling and parasympathetic regulation of heart rate as well as vision and motor function. The gene discussed is GNB5; the disease is gnb5-related intellectual disability-cardiac arrhythmia syndrome.