The coagulation factor XI (FXI) from the liver acts as an endocrine molecule in the heart, protecting it from heart failure. Scientists at the University of California, Los Angeles (UCLA) found that this communication between the two organs is mediated by the interaction between FXI and a heart protein. This interaction activated genes in cardiomyocytes that reduced inflammation, fibrosis and diastolic dysfunction, protecting the heart from a heart attack. That FXI participates in preventing heart failure suggests the possibility of using it as a therapeutic target.