These findings have been recapitulated in the genetically engineered PDA mouse models, where Kdm6a genetic deletion led to activation of the ΔNp63, Runx3 and Myc oncogenes and their related transcriptional network, which have all been implicated in the establishment of the basal-like PDA subtype and increased aggressiveness [8,13]. The gene discussed is KDM6A; the disease is Patent ductus arteriosus.