Of note, HIF-1α mediates the autophagic process induced by a hypoxic environment (Bellot et al, 2009), thus raising the interesting hypothesis that a defective HIF-1α induction/stabilization in CGD patients might be causally related to the impaired autophagy and that pharmacological stabilization of HIF-1α might restore LAP/DAPK1 and immune homeostasis during infection with CGD. Here, TGFB1 is linked to chronic granulomatous disease.