The molecular alterations found in our study in cardiac LECs during the development of HF include both seemingly adaptive changes, set to improve inflammatory resolution (upregulated chemokines, immune adhesion molecules, and MHC molecules), but also potential maladaptive changes that may contribute to lymphatic transport dysfunction (loss of lymphatic valves, reduction of Cldn5, Tjp1). The gene discussed is TJP1; the disease is hydrops fetalis.