On the flip side, the immune checkpoint molecules CTLA4 and PD-1 are inhibitory receptors expressed upon activated T cells, which bind with respective ligands expressed over DCs and MDSC and HCC cells [97,98]; the interaction not only suppresses cytotoxic activity of CD8+ T cells but also promotes tumour growth through increased signaling of the mammalian target of rapamycin (mTOR) independent of PI3K [99,100]. The gene discussed is CD8A; the disease is neoplasm.