HIF1α promotes the expression of immune checkpoint ligands such as PD-L1 on tumor cells, contributing to T cell exhaustion.240 Moreover, hypoxia causes the accumulation of adenosine, a metabolite that suppresses T cell activity.241 Additionally, metabolic pressure originating from mitochondria under hypoxic conditions accelerates terminal cell differentiation and increases ROS levels in T cells, leading to severe T cell dysfunction and failure.242. This evidence concerns the gene CD274 and neoplasm.