Identified key features included high levels of diacylglycerol kinase-α (DGK-α), low basal phosphorylation of the extracellular signal-regulated kinase (ERK) as well as reduced stimulation-induced phosphorylation of ERK, c-Jun N-terminal kinase (JNK) and AKT/protein kinase B. These features were caused by the tumor microenvironment as they were not observed in CD8-NILs or NK-NILs, and these lymphocytes were functionally active. This evidence concerns the gene AKT1 and neoplasm.