In addition, Immunohistochemical staining revealed no statistically significant differences in the expression of either CD68 or Ly‐6G between the C‐EVs‐treated mice and the N‐EVs‐treated mice, suggesting that tumor‐derived EVs may exacerbate cardiac injury through mechanisms independent of cardiac‐resident immune cells in I/R model (Figure S6, Supporting Information). This evidence concerns the gene CD68 and neoplasm.