We have identified rhodopsin as a therapeutic target for peripherin-2 associated diseases. Proof of concept studies were undertaken to demonstrate the application of this strategy across different peripheral-2 mutations using genetically modified animals. This strategy was then therapeutically translated using a previously characterized antisense oligonucleotide (see citations below) mRHO ASO1 to downregulate wild type rhodopsin levels in murine peripherin-2 patient disease models resulting in delayed disease progression.