In general, the disease-causing protein aggregates with ubiquitin in inclusion bodies disrupt the intermediate filament network and impairs the ability of the cell to degrade non-functioning proteins, which leads to photoreceptor apoptosis. Other mutations on rhodopsin lead to X-linked congenital stationary night blindness, mainly due to constitutive activation when the mutations occur around the chromophore binding pocket of rhodopsin. Several other pathological states relating to rhodopsin have been discovered including poor post-Golgi trafficking, dysregulated activation, rod outer segment instability, and arrestin binding [2][3].