Moreover, bone marrow transfer of Mark4-/- haematopoietic cells into wild-type mice (Extended Data Fig.1c; validation in Extended Data Fig.3a-3b) did not improve cardiac function after MI in comparison with the transfer of wild-type bone marrow cells (Fig.2d), indicating that the protective effect of MARK4 deficiency post-MI cannot be explained by the role of MARK4 in haematopoietic cells. This evidence concerns the gene MARK4 and myocardial infarction.