IRF5 and myocardial infarction: The relevance of cardiac M1 toward M2 MΦ phenotype transition for the resolution of inflammation and tissue repair post MI has recently been shown by Courties et al. (2014) [92] who demonstrated that in vivo silencing of the transcription factor IRF5, which is involved in inflammatory M1 MΦ polarization, supported resolution of inflammation, accelerated infarct healing, and attenuated development of post-MI HF.