In agreement with these findings, a recent study reported that iPSC differentiated from the neurons of patients with presenilin-1 (PS1) mutations display Ca2+ homeostasis failures and increased β-amyloid and p-Tau levels; negative allosteric modulators of RyR channels reverse these effects, reaffirming the importance of regulating RyR-mediated Ca2+ release in AD-affected neurons [72]. This evidence concerns the gene PSEN1 and Alzheimer disease.