The higher oxidative stress levels seen in DS fibroblasts in this work could increase the expression and activation of p53, one of the main effectors of p21 [51] and, interestingly, many of the neurodegenerative and immune defects of DS patients correlate with an increased apoptosis rate linked to an increased expression of the proapoptotic tumour suppressor p53 [52–54]. The gene discussed is CDKN1A; the disease is Dravet syndrome.