However, additional research is required to: (1) elaborate the molecular and cellular mechanisms that account for the decrease in BAG3 levels seen in hearts from patients with end-stage heart failure; (2) identify the effects of cardiac stress and left ventricular dysfunction on the chaperone and co-chaperone peptides that partner with BAG3 including the Hsp’s, sHsp’s, myopodin and synaptopodin; and (3) assess whether reconstitution of normal levels of BAG3 alone can interrupt the progression of heart failure. The gene discussed is SYNPO; the disease is heart failure.