Complementing the Hallmark gene-set analysis (Figure 4K), which showed up-regulation of inflammation-related gene sets in endothelial cells across all histologic features, these findings support the role of vascular inflammation and endothelial activation in HF progression.62 Furthermore, significant ligand-receptor interactions involving ACKR1 or CCL14 on the endothelial side correlated with fibrosis severity (see Supplementary data online, Figure S14). The gene discussed is CCL14; the disease is hydrops fetalis.