HMGA1 and glioblastoma: Alternatively, data from our laboratory have demonstrated that glucose reduction or caloric restriction-mimicking conditions shift brain tumor (glioblastoma) stem cells (BTSCs) towards an epithelial phenotype characterized by phospho-NUMB increased expression, supporting a bidirectional action between EMT and metabolism; this phenotype is reduced in HMGA1-high BTSCs [88], corroborating the role of HMGA1 as metabolic/EMT mediator.