A recent finding has revealed that HMGB1-3 s, a special form of HMGB1, in which non-oxidizable serine substitutes for all three cysteine residues, can interact with CXCR4 without CXCL12 and stimulate cardiac fibroblast migration in the context of myocardial infarction, worsening tissue remodeling after myocardial infarction (Di Maggio et al. 2017). This evidence concerns the gene CXCR4 and myocardial infarction.