MLH1 and neoplasm: There is growing evidence that distinct molecular entities in EC illicit different immune responses.11 12 EC that arise from a defective mismatch repair system (MMR), either through germline or somatic pathogenic variants in MLH1, MHS2(EPCAM), MSH6, PMS2 or their epigenetic controls (such as hypermethylation of the MLH1 promotor region, which is by far the most frequent) are known to have a high number of tumour infiltrating lymphocytes (TILs).11