Therefore, it is possible that some of the ocular defects associated with CHARGE syndrome are due to cell autonomous functions of CHD7 in retnal progenitor cells, whereas some ocular complications could result from non-cell autonomous mechanisms due to loss of CHD7 in cranial neural crest cells and/or the periocular mesenchyme, although the precise balance of mechanisms remain to be determined. This evidence concerns the gene CHD7 and CHARGE syndrome.