Upon T cell receptor (TCR) and leukocyte surface differentiation antigen 28 (CD28) stimulation, acylglycerol kinase (AGK) can be combined with phosphatase and tensin homolog (PTEN), which leads to phosphorylation of the lipid phosphatase PTEN and loss of its activity, thereby activating the phosphatidylinositol 3-kinase (PI3K) mechanistic target of rapamycin kinase (mTOR)-signaling pathway, promoting its glycolytic metabolism, and differentiating into effector T cells [337], exerting its anti-tumour effect. This evidence concerns the gene MTOR and neoplasm.