Since KIR2.1 protein expression and channel function become increased upon atrial fibrillation (e.g., Girmatsion et al., 2009) one can imagine that when Golgin-97 displays sufficient specificity for KIR2.1 channels in the atria, a potential drug target might be identified and warrants experimental follow up. The gene discussed is KCNJ2; the disease is atrial fibrillation.