In a murine MI model subjected to pre- and post-coronary artery occlusion, exogenous H2S treatment reduced the recruitment of CD11b+ Gr-1+ myeloid cells to the myocardium, inhibited their migration from the splenic reservoir, and decreased serum TNF-α and IL-1β levels, thereby protecting against ischemic myocardial injury (Zhang et al., 2014). This evidence concerns the gene TNF and myocardial infarction.