This must in turn be expected to lead to enhanced stimulation of tumour angiogenesis by PGH2 and PGE2 (and hence faster tumour growth), enhanced suppression of leukocytes important for antitumour immunological defense (such as NK cells, LAK cells and cytotoxic CD8+ cells) by PGE2, and more eicosanoid-induced pain at the same time as there might conceivably also be exacerbation of pain as a consequence of more oxidative activation of PKC isozymes in the C-fibres [90]. Here, CD8A is linked to neoplasm.