Another study concluded that HDAC4 plays an essential role in an acute increase of cardiac preload induced HDAC4 nuclear export, H3K9 demethylation, HP1 dissociation from the promoter region, and activation of the ANP gene and may represent a target for pharmacological interventions that prevent maladaptive remodeling in patients with HF [73]. The gene discussed is HDAC4; the disease is hydrops fetalis.