With the binding of PD-1 to PD-L1, tyrosine phosphatase is recruited to the cytoplasmic inhibitory motifs of PD-1 and dephosphorylates TCR, thereby inhibiting the downstream IFN, PI3K-AKT and Wnt/β-catenin signaling pathways to promote tumor progression (70, 71). This evidence concerns the gene AKT1 and neoplasm.