In agreement with the published literature (Oh et al, 2008; Ryu et al, 2014), we found that Tβ4 and HIF-1α crossregulate their reciprocal expression being the levels of HIF-1α defective in CGD mice but restored by Tβ4 and, conversely, silencing of HIF-1α in wild-type mice being associated with reduced levels of Tβ4. The gene discussed is HIF1A; the disease is chronic granulomatous disease.