While correcting one or both copies of a c.2299delG mutation in hiPSCs derived from an Usher Syndrome type 2 patient, Sanjurjo-Soriano and colleagues (2020) observed that this mutation leads to increased levels of mutant USH2A mRNA, therefore escaping the nonsense-mediated mRNA decay pathway that rids the cell from the toxic accumulation of truncated proteins; CRISPR/Cas9-mediated editing of the mutant USH2A sequence resulted in expression levels that were similar to those in control hiPSCs [102]. This evidence concerns the gene USH2A and Usher syndrome type 2.