Previous study showed that CFH controls intracellular C3 levels of macrophages in a cell‐autonomous manner and negatively regulates consumption of complement component 3 (C3), thereby restricting the complement activation,[61] improve TNF‐α‐induced inflammation in rheumatoid joint inflammation,[62] and inhibit vascular endothelial cell migration and anti‐angiogenesis in tumor cells.[63] This is consistent with our observation of lower vascularity score in repaired tendons in the ACM group (Figure S4A, Supporting Information). Here, TNF is linked to neoplasm.