Although HIF‐1α is known to play a key role in the protection from acute ischemia (Bernhardt et al., 2006; Ma et al., 2009; Matsumoto et al., 2003), recent evidence suggested that prolonged unregulated activation of HIF‐1α could enhance maladaptive responses, which lead to glomerulosclerosis and interstitial fibrosis in multiple animal models. This evidence concerns the gene HIF1A and glomerulosclerosis.