Notably, targeting the A2BR pathway seems sufficient to mitigate effector CD8+ T cell exhaustion (as determined by reduced expression of PD-1, TOX, and CD39 within tumors), linking to enhanced levels of GSH/GPX4, which is supported by an elegant study showing the importance of CD39 and adenosine signaling for suppressive function of tumor-infiltrating exhausted T cells in the hypoxia tumor microenvironment (50). This evidence concerns the gene GPX4 and neoplasm.