In DCM, elevated β-hydroxybutyric acid (βOHB) levels promote epigenetic activation of the lipocalin-2 (Lcn2) promoter via H3K9bhb modification, leading to nuclear translocation of the NF-κB/RPS3 complex and initiating proinflammatory and profibrotic gene expression programs [148]. The gene discussed is LCN2; the disease is familial dilated cardiomyopathy.