Here we provide evidence that normalization of diabetes-induced Ca2+ dyshomeostasis in diabetic hearts, through restoration of the sarco/endoplasmic reticulum Ca2+-ATPase (Serca2a) function, significantly suppressed resistin expression via inhibition of NFATc and enhanced the activity of AMP-activated protein kinase (AMPK), a downstream target of resistin signaling. Here, NFATC1 is linked to diabetes mellitus.