Indirect evidence for MMT includes the co‐localization of α‐SMA (a marker specific to activated fibroblasts) with macrophage markers (F4/80 or CD68), indicating that macrophages expressing α‐SMA are MMT cells.[29] Direct evidence of MMT is provided by lineage tracing and fate mapping experiments, which label and track bone marrow‐derived macrophages.[16] Although our study finds that MMT cells constitute only ≈30% of all myofibroblasts—significantly lower than the over 50% reported in renal fibrosis[14, 16, 26]—this discrepancy may be due to differing definitions of myofibroblasts. The gene discussed is ACTA1; the disease is renal fibrosis.