Unlike adult mammals, adult zebrafish can regenerate injured heart tissue. Heart regeneration in zebrafish is known to involve partial de-differentiation and proliferation of cardiomyocytes, but are cardiomyocytes involved in any other processes during heart repair? Here (p. 4133), Yasuhiko Kawakami and co-workers report that cardiomyocyte migration to the injury site is required for zebrafish heart regeneration. Ventricular amputation, they report, induces expression of the chemokine ligand cxcl12a and the chemokine receptor cxcr4b in epicardial tissue and cardiomyocytes, respectively. Both pharmacological inhibition of Cxcr4 function and genetic loss of cxcr4b function prevent heart regeneration, they show, and lead to mislocalisation of proliferating cardiomyocytes outside the injury site without affecting cardiomyocyte proliferation. Finally, the researchers use a photoconvertible fluorescent marker to show that, although cardiomyocytes migrate into the injury site in control hearts, their migration is inhibited in Cxcr4-antagonist-treated hearts. Thus, cardiomyocyte migration into injured zebrafish heart tissue is regulated independently of cardiomyocyte proliferation, and coordination of both processes is essential for heart regeneration.