Li et al. showed the physiological of peroxisome proliferator-activated receptor γ(PPARγ) and DNA damage response (DDR) by using pulmonary arterial hypertension (PAH) as a model that impaired PPARγ signalling pathway related to endothelial cell dysfunction and disrupted PPARγ-UBR5 (MRE11-RAD50-NBS1) interaction, heightened ATM interactor (ATMIN) expression and DNA lesions. This evidence concerns the gene UBR5 and pulmonary arterial hypertension.