While stable CaV2.2 mRNA and protein levels typically result in increased N-type Ca2+ currents in the SG neurons of rats with heart failure, pointing to possible post-translational modifications [36], similar changes in VDCC expression and currents were not observed in the SG neurons of cirrhotic rats, thus dissociating them from cellular hyperexcitability. The gene discussed is CACNA1B; the disease is heart failure.