In line with our serum deprivation study [14], the present study also demonstrate TGF-β1 could partially reverse the toxicant effects of H2O2 on the viability of AF cells by inhibiting autophagy (showing reduced GFP-LC3 autophagosomes accompanied with decreased expressions of Beclin-1 and LC3 II/I and increased p62) and apoptosis (showing reduced expression of caspase-9 and caspase-3, Bax/Bcl-2, the ratio of cytoplasmic/mitochondrial cyt-C and MMP) at the early stage (0.5–4 h), preliminarily revealing that the supplementation of TGF-β1 may be an underlying treatment approach for IVDD [26]. Here, TGFB1 is linked to atrial fibrillation.