β2 M downregulation, as a resistance mechanism to ICT, is restricted to tumour cells that have reduced tumour-antigen presentation via MHC class I. Therefore, existing clonally expanded anti-tumour CD8 + T cells, which are eventually able to reach the tumour site, will have a reduced tumour-antigen interaction via MHC class I and TCR, in addition to co-stimulatory molecules, reaching poor activation signals, which ultimately results in drastic T-cell proliferation suppression [56]. Here, CD8A is linked to neoplasm.