Iron-overload alone does not seem to explain the pathogenesis of heart failure (HF) associated with beta-thalassemia major (BTM). Further contributing factors i.e. myocarditis, HLA haplotypes are being claimed to play important roles in the development of HF especially in case of predominantly left-sided involvements. Here we report a case of BTM plus secondary hemochromatosis, in whom the testosteron replacement therapy was temporally associated with initiation and aggrevation of HF. We propose that gonadal replacement therapy can be considered as a potential contributing factor to the heterogenous and multifactorial nature of BTM-associated HF.