In mice, loss of the transcription factor, Prox1, a gene necessary for specification and maintenance of LECs,12 resulted in muscular septal defects and hypoplastic ventricles.13 Similarly, knockout of Podoplanin, which is necessary to segregate the blood and lymphatic vasculature,14–16 resulted in myocardial defects and cardiac anomalies, as well as chylothorax.16,17 These results suggest that there may be subclinical intrinsic LEC defects that contribute to the development of postoperative chylothorax. The gene discussed is PDPN; the disease is Chylothorax.