HSF1 was demonstrated as a key factor involved in the adaptive mechanism of transition from adaptive cardiac hypertrophy to maladaptive heart failure,6 as well as an essential intrinsic factor protecting the cardiomyocytes against ischaemic injury via interacting with STAT3.5, 7 In the present study, our first finding is that HSF1 phosphorylation was inhibited by the ischaemic stimulation. The gene discussed is STAT3; the disease is cardiac hypertrophy.