In injured neonatal hearts, MYDGF derived from endothelial cells, rather than macrophages, promoted cardiomyocyte proliferation and improved heart regeneration.[13] In the kidney, the expression of MYDGF in renal tubules was higher than that in macrophages in healthy mice based on the data from the publicly available single‐cell datasets, suggesting that tubular MYDGF might play an important role in maintaining kidney homeostasis.[14] However, the expression pattern and the role of tubular MYDGF in CKD remain unclear. Here, MYDGF is linked to chronic kidney disease.