Given the strong role of PS externalization in mediating erythrophagocytosis and procoagulant effects and a wide array of upstream signaling pathways resulting in PS exposure (Ca2+ signaling, caspase-3, ROS, or ceramide), including in liver diseases, targeting PS exposed on the cell surface rather than the key signaling components of eryptosis seems to be a more effective pharmacological strategy. Here, CASP3 is linked to liver disorder.