Tumours achieve immune escape from cytolytic T cell immunosurveillance, in part via loss of heterozygosity (LOH) of the human leucocyte antigen (HLA) cluster, an immunoediting strategy that reduces antigen expression via the major histocompatibility complex (MHC), to escape T cell receptor-dependent CD8 lymphocyte mediated tumour suppression. This evidence concerns the gene HLA-C and neoplasm.