A daptive and deficient growth of cardiac mus-cle-illustrated, respectively, by hypertrophy after a hemodynamic load and by intractable pump failure after myocardial infarction-impose fundamental limits to contemporary clinical cardiology. Relatively little is known of the signaling molecules in the myocardium that might coordinate cardiac growth and morphogenesis during fetal life, communicate growth signals from the sur-face membrane to the nucleus, interact with genomic DNA to impel cell growth and alter the synthesis of muscle proteins, and, eventually, extinguish the ability of cardiac myocytes to proliferate. Potential can-didates as regulators of myocardial growth anddifferentiation are the polypeptide growth factors, 12 multifunctional proteins analogous to but distinct from the classic (hematogenous) hormones. The initial discovery of peptide growth factors can be traced to the fundamental observation that extracts of mouse submaxillary salivary gland support growth of the innervating sympathetic neurons. 3 Subsequent purification of nerve and epidermal growth factors gave impetus to the search for other trophic com-pounds, to pursuit of their pleiotropic effects on cell growth and maturation, and to delineation of cellular pathways for growth factor signal transduction. Cardiac myocytes recently were demonstrated to be targets for theaction of at least two sets of growth factors, 4 the heparin-binding" fibroblast" growth fac-tors (FGFs) 2 and the type, B transforming growth factors (TGFI3s), l which are the emphasis of this