Role of Ca2+ ATPase as energy sensors, mTOR and AKT as kinases and NFkB as cell survival factor in stabilisation of the redox regulation under VIT-E and/or CRM administration in hyper-thyroid states may be useful in mitigating cardiac damage under altered thyroid states in general and reducing the risk of hyperthyroidism induced heart failure or stroke in particular. The gene discussed is AKT1; the disease is hyperthyroidism.