Thus, it appears that this increase of sPLA2-IIA and -IB proteins due to their defective clearance contributes to exacerbation of autoimmune myocarditis, although it remains unclear whether these sPLA2s act through PGE2 synthesis or through other mechanisms, whether some other sPLA2s that are expressed in the myocardium and have the capacity to bind to PLA2R1 are also involved in this process, or whether the effect of PLA2R1 ablation is sPLA2-independent. This evidence concerns the gene PLA2G2D and autoimmune myocarditis.