This effect was illustrated in a series of experiments from Xander Wehrens’ lab in which knock-in mice with constitutively activated RyR2-S2367D were more resistant to pacing-induced atrial fibrillation (AFib), while knock-in mice with a non-phosphorylatable alanine substitution at that same site (RyR2-S2367A) were more susceptible to AFib (Campbell et al., 2020). The gene discussed is RYR2; the disease is atrial fibrillation.