The large amount of ROS generated after cerebral infarction promotes HMGB1 transfer by oxidizing the “‐SH” group of cysteine at position 106 in the nucleus, which promotes HMGB1 translocation to the cytoplasm, wherein cytoplasmic HMGB1 binds competitively to beclin1, eventually disrupting the interaction between beclin1 and B‐cell lymphoma‐2 (Bcl‐2) and promoting autophagy (Pan et al., 2020; Tang et al., 2010, 2016). Here, HMGB1 is linked to brain infarction.