Since leukotriene D4 (LTD4), the substrate of Dpep2, and its hydrolysate LTE4 have been reported to act as pro-inflammatory lipid mediators (Habib et al., 2003; Steinke et al., 2014; Bankova et al., 2016), and we observed the increase of cardiac LTE4 level in mice with CVB3-induced myocarditis (Figure 5A), we firstly deduced that Dpep2 might modulate macrophage inflammation by LTE4. Here, DPEP2 is linked to myocarditis.