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. The gene discussed is CYLD; the disease is hydrops fetalis.