In endothelial cell-bone morphogenetic protein type 2 receptor-knockout mice unable to stabilise p53 in endothelial cells under oxidative stress, nutlin-3 rescued endothelial p53 and PPARγ-p53 complex formation and induced target genes, such as APLN and JAG1, to regenerate pulmonary microvessels and reverse pulmonary hypertension [40]. The gene discussed is TP53; the disease is pulmonary hypertension.