It should be noted that neutrophil-specific Wnt5a deletion protects the heart from pressure overload–induced dysfunction (Wang et al. 2019) and loss of macrophage Wnt secretion improves contractile dysfunction after MI (Palevski et al. 2017), indicating a significant role of Wnt ligands derived from both myocytes and non-myocytes in heart failure progression. The gene discussed is WNT5A; the disease is heart failure.