(b) Our findings broadly support the findings of another study in this area linking GAS5 to myocardial infarction (MI), which found reduced GAS5 transcript levels in the hearts of MI-modeled mice [30], and that induced GAS5 may be able to reduce cardiomyocyte apoptosis caused by MI by downregulating Semaphorin (sema3a), a secretory protein that could reduce inflammation and improve cardiac function after MI by promoting inflammation resolution [9]. Here, GAS5 is linked to myocardial infarction.