More specifically, T3 regulates myocardial contraction/relaxation in MI by inducing the pathological switch of myosin heavy chains (MHC) from α to β isoform, and controls calcium ions (Ca2+) flux into the sarcoplasmic reticulum by inducing expression of sarcoplasmic reticulum calcium adenosine triphosphatase (SERCA2) and inhibiting phospholamban (PLB), SERCA’s counteracting molecule (Kinugawa et al., 2001). This evidence concerns the gene PLN and myocardial infarction.