Thus, we can now consider CaMKII a leading target for therapeutic development in terms of arresting the progression of optic neuropathies, especially since similar findings have been replicated across three different institutions [Mount Sinai Health System (Guo et al., 2021) and herein Boston Children's Hospital and Stanford University], using three different mouse strains [C57BL/6J (Guo et al., 2021), 129X1/SvJ, and 129S1] and using AAV vectors with different capsids and promoters. This evidence concerns the gene CAMK2G and Optic neuropathy.