Normalized FMR-1 gene expression was achieved by CRISPR/Cas9-mediated deletion of the CGG repeat in hiPSCs from fragile X syndrome patients, a change that was sustained even after differentiation into neural progenitor cells (NPCs) and mature neurons; in addition, hypermethylation of the CpG sites upstream of FMR-1 was reversed [128]. The gene discussed is FMR1; the disease is fragile X syndrome.