In addition, both azelnidipine (ALP), a dihydropyridine calcium channel blocker known for its treatment of hypertension and methylarachidonyl fluorophosphate (MAFP), a cPLA2 inhibitor, also suppressed oAβ-induced translocation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) p65 subunit to nuclei in cerebral endothelial cells, suggesting that cPLA2 activation and calcium influx are essential for oAβ-induced NFκB inflammation [53]. The gene discussed is NFKB1; the disease is Hypertension.