MIAT and myocardial infarction: Given our findings that HOXA4 was a crucial target of MIAT [8] and several apoptotic and fibrotic genes are activated by CM-derived MIAT (Figs. 1D, 4, and 6), circulating levels of MIAT in post-MI patients could be used to guide current and future targeted treatment options by modulating the downstream targets of MIAT.