TNFSF11 and myocardial infarction: Global RANKL inhibition or inhibition of RANKL derived from mesenchymal cellular sources using a monoclonal anti-RANKL antibody did not significantly alter cardiac function post-MI, whereas specific inhibition of RANKL derived from hematopoietic cellular sources improved post-ischemic cardiac function, reduced mortality, and downregulated post-ischemic production of inflammatory cytokines.