In addition, Chen et al. demonstrated, in 2019, that LRRC8A is upregulated in cardiac fibrosis following myocardial infarction (MI), and the cardiac-specific LRRC8A knockdown ameliorates the post-MI cardiac fibrosis and ventricular dysfunction via the JAK2-STAT3 signaling pathway [30]. This evidence concerns the gene LRRC8A and myocardial infarction.