NFKB1 and heart failure: 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.