During this process, the phosphorylation of microtubule-associated protein 4 by microtubule-affinity-regulating kinase 4 (MARK4) gives VASHs more access to detyrosinating α-tubulin, and the loss of ejection fraction is markedly reduced in the absence of MARK4 in an acute myocardial infarction model [117]. Here, MARK4 is linked to myocardial infarction.