Muscle defects associated with Apobec2 deficiency have been also documented in zebrafish by using morpholino oligonucleotide–mediated knockdown of the Apobec2 proteins (Apo2a and Apo2b), which demonstrated myopathy in the somitic musculature (evidenced by the presence of cell-free spaces, long myofibers, and impaired heart function) (13). This evidence concerns the gene APOBEC2 and myopathy.