models via repression of Nav1.7, a pain gatekeeper gene. Our approach is completely different from previous attempts. Rather than targeting the protein or the RNA, which undergo extensive turnover, we target the DNA of Nav1.7 to downregulate the channel without introducing permanent mutations in the genome. Our co-lead program is a mutation agnostic approach to tackle all forms of retinitis pigmentosa, preventing neuronal degeneration in the eye through in vivo cellular reprogramming. We secured more than $8M in grants from the NIH and CIRM and with a strong IP portfolio internally developed and in-licensed from UCSD, we are well poised to create the medicines of the future.