HMGA2 and neoplasm: Although the etiology remains elusive, some progress has been made about the molecular mechanisms involved in tumour initiation and growth including (1) steroid hormone–dependency2, (2) excessive accumulation of extracellular matrix (ECM), a reservoir for growth factors, cytokines, chemokines, angiogenic and inflammatory response mediators and proteases that contribute to cell growth, differentiation and ECM turnover5,6 and (3) alterations in driver genes such as HMGA2 (high mobility group AT-hook 2) and MED12 (mediator complex subunit 12) occurring in most of the tumours7,8.