Mice expressing heat shock transcription factor-1 (HSF-1) exhibiting reduced endothelial p53 expression were characterized by increased angiogenesis and cardiac HIF1α expression and protected against pressure overload-induced heart failure, whereas HSF1 deficient mice exhibit aggravated cardiac remodeling under pressure overload due to impaired, imbalanced angiogenesis (241). The gene discussed is HIF1A; the disease is heart failure.