TP63 and Patent ductus arteriosus: 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.