Furthermore cluster-1 mutations, related to tumor “pseudohypoxia” under normoxic conditions, have always been claimed to prevent immune system recognition by interfering with T cell effector function, impairing tumor infiltration, activating immune-suppressive monocytes and increasing the expression of PDL1 and its receptor, thus resulting in immune suppression and tolerance [10,79,80]. The gene discussed is CD274; the disease is neoplasm.