In vitro studies have demonstrated that SIRT6 deacetylates the STING protein, resulting in decreased ubiquitination and a stabilized STING protein, while in a murine model of MI, STING inhibition has led to alleviated cardiac dysfunction and adverse remodeling by inhibiting the release of pro-inflammatory cytokines post-MI [44]. This evidence concerns the gene STING1 and myocardial infarction.