FANCD2 and Friedreich ataxia: A different strategy aimed to create a frameshift restoration in the FANCA c.295 C >T FA patient lymphoblastoid cell line (LCL) using CRISPR-Cas9-induced NHEJ created a 21 base pair deletion, allowing the production of the functional FANCA protein as shown by FANCD2 foci formation and resistance to MMC; however the initial therapeutic insertions/deletions (indels) were as low as 2.3% [14].