Contrary to this hypothesis, Wei et al. have reported that endothelial deletion of HIF-1α, achieved by the Tie2-Cre driver instead of the Cdh5-Cre as in our study, leads to aggravated cardiac hypertrophy in mice exposed to pressure overload, which the authors attribute to increased apoptosis of cardiomyocytes (Wei et al., 2012); it remains to be determined whether macrophage infiltration in the myocardium is altered. This evidence concerns the gene HIF1A and cardiac hypertrophy.