However, in a recent study investigating the contribution of the IP3R and RyR to the reported altered endothelial function and plausible mechanisms underlying the immunosuppressant-mediated hypertension and endothelial dysfunction in organ transplant patients, Buckley et al. (2020) [45] suggested that the increase in IP3-evoked Ca2+ release generated by TAC tacrolimus is mediated by an effect of the drug on calcineurin rather than FKBP modulation itself [45]. This evidence concerns the gene ITPR1 and endothelial dysfunction.