The pathological significance of the aforementioned signaling pathways that mitochondrial dysfunction can trigger caspase-3-dependent PKCδ activation is further illustrated by multiple PD model systems demonstrating that it translocates to the nuclear membrane and functions as a kinase to phosphorylate Lamin B1 at the T575 residue, resulting in the loss of Lamin B1 and hence damaging the nuclear membrane’s structural integrity followed by the subsequent apoptotic death of the DAergic neurons (Figures 9A,B). The gene discussed is CASP3; the disease is Parkinson disease.