To examine whether stabilization of RyR2 through enhanced CaM binding is critical for AD pathogenesis, we generated AppNL-G-F/RyR2V3599K double homozygous mice (AppNL-G-F/RyR2V3599K mice), and evaluated how the AD phenotype is modified (Supplementary Fig. 1). The gene discussed is RYR2; the disease is Alzheimer disease.