Since we detected an increase in both Parkin expression and formation of giant Parkin-rich areas in HF myocytes, but a decrease in MFN2 expression (Figure 3), we hypothesized that a decrease in MFN2-mediated mito-ER contact sites impairs mitophagy under conditions of enhanced Parkin recruitment, leading to the formation of Parkin-rich areas with dysfunctional mitochondria (see Figures 2, 4). This evidence concerns the gene MFN2 and hydrops fetalis.