Although the specific mechanism underlying the diastolic Ca2+ alterations in T2D cardiomyocytes have not been established yet, cardiac dysfunction in diabetes has been associated with detrimental expression of the sarcoplasmic reticulum Ca2+ pump SERCA2 (Belke et al., 2004; Suarez et al., 2008) and an aberrant ryanodine receptor Ca2+ leak (Santulli et al., 2015). This evidence concerns the gene ATP2A2 and type 2 diabetes mellitus.