Our prior data show that the expression levels of the total H3 itself increased in both MitoPark mice and postmortem tissues of PD patients compared to the non-disease groups (data not shown), in alignment with another recently published human PD study (Toker et al., 2019), therefore we used both β-actin and H3 as loading controls in this study. The gene discussed is ACTB; the disease is Parkinson disease.