Myocardial hypertrophy was observed in male mice with null mutations of CD38, and FKBP12.6, a cADPR binding protein146,147) and the altered stoichiometry of FKBP12.6 versus type 2 RyR as a cause of abnormal Ca2+ leak through RyR in heart failure in man.148) As diabetic complications in the cardiovascular system are frequently observed, screening of the abnormalities in the CD38-cADPR signal system may provide a clue for the underlying molecular mechanism. The gene discussed is FKBP1B; the disease is cardiac hypertrophy.