This increased adenosine prevents rapid phosphorylation of the ZAP70 kinase as well as AKT and ERK1/2 in T cells.325 This leads to the inhibition of effector T cell and NK-cell functions, enhances Treg function and proliferation, reducing the ability of Tregs to mount effective antitumor responses.326 Consequently, targeting the CD39/CD73-adenosine pathway has emerged as a promising therapeutic strategy to reverse immunosuppression, enhance antitumor immunity, and potentially improve clinical outcomes in GBM (Fig. 6). The gene discussed is AKT1; the disease is glioblastoma.