Indeed, there are data to suggest that cardiac hypertrophy seen with TZDs may involve PPARγ-dependent and independent pathways, since cardiomyocyte-specific PPARγ-knockout mice were shown to develop cardiac hypertrophy and treatment of both wild-type and knockout mice with rosiglitazone also induced cardiac hypertrophy [49]. The gene discussed is PPARG; the disease is cardiac hypertrophy.