Numerous studies have consistently demonstrated that increased apoptosis contributes to the development of myocardial infarction and heart failure, whereas interventions aimed at limiting apoptosis can provide protection for the heart.[5] For instance, Li et al[31] found that under the stimulation of H/R or DOX, miR-181c can down-regulate the protein expression of Fas, IL-6 and Tnf-α, and up-regulate the phosphorylation of Bcl-2 and Akt. Here, IL6 is linked to heart failure.