In a mouse model of middle cerebral artery occlusion (MCAO), HMGB1 was present predominantly in the form of reduced‐HMGB1 in serum, with the level of disulfide‐HMGB1 being extremely low at 2 h after cerebral infarction; however, a gradual increase in the serum disulfide‐HMGB1 concentration was observed with an increase in the infarction duration (Liesz et al., 2015). This evidence concerns the gene HMGB1 and cerebral infarction.