NFATC2 and type 2 diabetes mellitus: Our study is the first to explore the possible role between FAP and this pathway and to find that the abnormal increase of FAP activates the CaMKIIδ-Calcineurin A-NFATc2 signaling pathway independent of glycemic control (Figure 6a and b), thereby leading to the pathophysiological manifestations of T2DM-induced HFpEF and diastolic dysfunction [37–39].