Although we found that HCN4 does not form complexes with PP2A in NRVMs, implying that PP2A-related dephosphorylation of HCN channels may not participate in SGO1 mediated HCN4 regulation, a whole range of other signaling pathways should be assessed for their potential involvement in If-regulation in the CAID Syndrome. The gene discussed is SGO1; the disease is chronic atrial and intestinal dysrhythmia.