AKT1 and neoplasm: PD‐1 is expressed on chronically stimulated T cells [99], and upon engagement with PD‐L1—expressed on tumor cells, endothelial cells, DCs, and other immune subsets—it recruits SHP‐2 phosphatase, leading to dephosphorylation of key TCR signaling intermediates including ZAP70, PI3K/Akt, and mTOR [100].