The main conclusions of this paper are that (i) the BH4 domains of Bcl-2 and Bcl-XL suppress physiological RyR-mediated Ca2+ release in isolated PACs exposed to the hormone CCK; (ii) the Ca2+-signaling-inhibitory properties of these BH4 domains can be utilized to dampen pathophysiological RyR-mediated cytosolic Ca2+ overload associated with AP, protecting PACs against necrosis. This evidence concerns the gene BCL2 and alkaline phosphatase measurement.