Since increased phosphorylation of phospholamban (PLB) at Serine 16 (S16), mediated by protein kinase A, and PLB at Threonine 17 (T17), mediated by calmodulin-dependent kinase II (CaMKII) has been suggested to contribute to altered calcium responsiveness to beta-adrenergic signaling in cardiac hypertrophy [22,23], the phosphorylation status of these PLB sites were assessed. This evidence concerns the gene PLN and cardiac hypertrophy.