To obtain a new transgenic mouse highly expressing an active variant of 1 type Na+/Ca2+ exchange transporter myocardially specifically and to provide a screening system for a dilated cardiomyopathy therapy using the mouse.

The transgenic mouse for reproducing pathologic findings and ultrasonic electrocardiograph findings of dilated cardiomyopathy is obtained by gene transfer of active type NCX1 protein having variation deleted in Na+ inactivation mechanism to a mouse by using a myocardially specific promoter. The transgenic mouse is useful for a screening system of a pharmacotherapy and a gene therapy of dilated cardiomyopathy.