Indeed, a recently published study on PCSK9 knock-out mice found that PCSK9 deficiency could negatively affect cardiac lipid metabolism (increased left ventricular thickness and an increased cardiac accumulation of lipid droplets were associated with a reduced density of mitochondrial cristae leading to impaired oxidative phosphorylation and mitochondrial metabolism) in a LDLR-independent manner, contributing to the development of HF and secondarily to high NPs levels [35]. Here, LDLR is linked to hydrops fetalis.