Moreover, when cells were treated with 2 mM β-OHB and 1 μM TAT-MP1Gly simultaneously, we observed further increase in Parkin puncta and LC3-mediated autophagosome formation in HF myocytes, indicating that β-OHB stimulates Parkin translocation in both aging and HF; however, in conditions of impaired MFN2-mediated content exchange and trafficking, β-OHB seems to enhance (Figure 6C) formation of Parkin-rich areas in mitochondria. The gene discussed is MAP1LC3A; the disease is hydrops fetalis.