Interestingly, atrial fibrillation in patients was accompanied by an increase of A2A-ARs on mRNA and protein level in atrial tissue and an increase in cardiac ryanodine receptor (RYR2) phosphorylation, and this was suggested to lead to an altered flow of Ca2+ through the sarcolemmal sodium calcium exchanger (NCX) and thus arrhythmias (Llach et al., 2011a). The gene discussed is TLX2; the disease is atrial fibrillation.