HMGA2 and neoplasm: The functional footprint of these losses is coherent with known tumor-suppressive circuits in EC such as diminished let-7 which permits HMGA2/RAS–MYC activity, reduced hsa-miR-34a which weakens p53-dependent control and associates with invasive traits, and loss of hsa-miR-200b which relaxes repression of ZEB1/2 and EMT [30].