DCs act as an effective immune regulator during the post‐infarction healing process via its regulation of immune cells homeostasis.25 In addition, high expression of IL‐36R, the membrane receptor for IL‐36, IL‐36Ra and IL‐38, was detected on DCs.14 These reach results prompted us to investigate whether IL‐38 acts on DCs and therefore plays a further role on T lymphocytes. This evidence concerns the gene IL1RL2 and infarction.