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In situ reprogramming of rod photoreceptors. Rods may be reprogrammed in early stage IRDs to generate ‘pseudocones’ through manipulation of the NRL and NR2E3 transcription factors which normally determine rod fate (e.g., by CRISPR-mediated gene knockout or molecular inhibitors, PR1 and PR3). Pseudocones confer resistance against rod-specific gene mutations, thus slowing the rate of retinal degeneration.
