Upon pathogen infection or oxidative stress, the mitochondrial membrane permeability transition pore (MPTP) is opened, and the cytoplasmic cytC binds to Apaf-1 to form apoptotic bodies, which subsequently forms an apoptotic complex via binding to caspase-9, resulting in transmission of signals to downstream effector (caspase3) and initiation of apoptosis [40]. This evidence concerns the gene APAF1 and infection.