Our previous work suggests that cone photoreceptor inner segment (CIS) mitochondria demand and produce more ATP than rods. The CISs utilize two complimentary strategies to increase ATP production: increase the absolute number of mitochondria and their cristae surface membrane area. In this treatise, we ask: How are crista junctions formed and regulated? Once formed, are there physical mechanisms that constrain their diameter? How are the constrictions in cristae regulated and is this key for cytochrome c release during apoptosis? What are their differences in rod and cone susceptibility to apoptotic cell death during calcium overload and oxidative stress?