Although our study is the first to our knowledge to designate misregulation of MMP9 as a crucial effector of RA-induced OFT defects, exogenous RA signaling promotes MMP9 expression in several other developmental and disease contexts, including dendritic cell migration [60], neuroblastoma [43,44], and glomerulosclerosis [45]. This evidence concerns the gene MMP9 and glomerulosclerosis.