LMP1 can utilize the PI3K–AKT–mTOR pathway for inducing CD137 expression to support growth of the Hodgkin and Reed/Sternberg (HRS) cells and escape from immune surveillance [92]; it can also promote tumor immune escape by upregulating tumor cell PD-L1 through the NF–κB pathway in extranodal natural killer/T-cell lymphoma (ENKTL) [93]. This evidence concerns the gene MTOR and neoplasm.