We then identified PARP-1 as playing a key role in CDD repair and maintaining cell survival under these conditions [13], and which is supported by our current study revealing that PARG depletion/inhibition plays a similar role, suggesting that poly(ADP-ribosyl)ation controlled by PARP enzymes and PARG are critical in this process. This evidence concerns the gene PARP1 and craniodiaphyseal dysplasia.