GNB5 and Bradycardia: We studied for the first time the cellular electrophysiological consequences of human genetic variation in GNB5. We demonstrated that the Gβ5-S81L variant in the homozygous state results in an increased IK,ACh density upon muscarinic receptor stimulation and excessive slowing of spontaneous activity, a plausible mechanism for the bradycardia observed in the patients.