Accordingly, we employed three protocols aimed to determine whether the AA-deficient treatments (causing arrhythmias) affect intracellular Ca2+ handling, which results in elevated [Ca2+]i: (i) measuring Ca2+ transients and caffeine-induced RyR-mediated sarcoplasmic reticulum (SR) Ca2+ release; (ii) testing the ability of rapid pacing to cause arrhythmias; and (iii) testing the involvement of NCX in the arrhythmias caused by -AA+YWF. The gene discussed is TLX2; the disease is cardiac arrhythmia.