MSI-high tumours have defects in the DNA mismatch-repair pathway, most commonly due to epigenetic silencing of the MutL homolog 1 (MLH1) gene or inactivation of MSH2, and consequently accrue extensive genomic mutations that lead to the expression of neoantigens by the tumours, and their immune recognition by neo-antigen specific cytotoxic T cells (72, 73). This evidence concerns the gene MSH2 and neoplasm.