Hence, a majority of the in vivo gene therapy approaches for retinal dystrophies rely on the CRISPR-Cas-mediated NHEJ pathway.78–86 Another genome editing strategy, namely, homology-independent targeted integration (HITI), was utilized to successfully knock in exon 2 of Mertk (MER/AXL/TYRO3 receptor kinase) gene, thereby protecting from retinal degeneration.87 HITI exploits the NHEJ repair mechanism and enables targeted transgene insertion without the need of an HR donor template in dividing and nondividing cells. The gene discussed is MERTK; the disease is inherited retinal dystrophy.