For example, pre-clinical studies in rats have shown that testosterone deficiency can pre-dispose to arrhythmias, which can be prevented by testosterone-replacement due to a stabilization of the ryanodine receptor 2,42 while we observed evidence of higher frequency and incidence of DAD in male rabbits’ atrial CMs, similarly as reported by Tsai et al.43 and pro-arrhythmic DAD facilitating effects of testosterone. This evidence concerns the gene RYR2 and hyperinsulinemic hypoglycemia, familial, 4.