The compartment-specific dysregulation of CYLD, a known regulator of T-cell receptor signalling and NF-κB activation, may underlie the transition from acute inflammatory responses to maladaptive immune remodelling during HF progression; its dual role in cardiomyocyte survival pathways and lymphocyte activation could explain its superior diagnostic performance compared with that of conventional myocardial stress markers. Here, NFKB1 is linked to hydrops fetalis.