The molecular mechanism involved in Dox-induced cardiotoxicity has been proposed to account for increasing reactive oxygen species (ROS) production, caspase activation, altered calcium handling and mitochondrial injury.16, 17 It was demonstrated that transgenic mice with cardiac-specific overexpression of STAT3 gene are protected against Dox-induced cardiomyopathy.18 Therefore, understanding how STAT3 activation can be modulated would provide new opportunities to develop effective therapeutics for Dox cardiotoxicity. This evidence concerns the gene STAT3 and cardiomyopathy.