Several studies performed in vitro indicated that BNP can inhibit monocyte chemotaxis [135], deplete the number of monocytes, B lymphocytes, and NK cells in cultured human peripheral blood mononuclear cells [136], and regulate the production of a wealth of inflammatory molecules by human macrophages [137, 138]. In vivo, a study using transgenic mice overexpressing BNP reported increased cardiac neutrophil infiltration and MMP-9 expression after MI in transgenic animals, pointing to a key role of BNP in the processes of matrix remodeling and wound healing in this setting [138]. This evidence concerns the gene NPPB and myocardial infarction.