Aberrant expressions of transcription factors (TFs) and the subsequent alterations in epigenetic landscapes may be responsible for the fluctuations of transcriptional programs during cancer progression.[4] For example, through modulating enhancer activities, TF TP63 is capable to activate the transcriptional programs of squamous PDA subtype, leading to an aggressive cancer phenotype.[5] Until recently, studying the dynamic changes of transcriptional programs as the cancer progresses has been difficult due to lack of in vitro PDA progression models for different stages of PDA. The gene discussed is TF; the disease is Patent ductus arteriosus.