It has been demonstrated that NRF2/TRX1 and HIF-1α levels increased in adenocarcinoma cells due to oxidative stress induced by intermittent hypoxia in the NOX1-dependent pathway [99], and CO increased HIF-1α concentration through translational stimulation and stabilization of this protein in human umbilical vein endothelial cells and primary human brain astrocytes [100]. Here, HIF1A is linked to adenocarcinoma.