Our findings are corroborated by recent evidence that STAT3 and STAT5 are constitutively activated in malignant cells, and that their persistent activation facilitates cancer development and progression by altering downstream gene expression through epigenetic modification, EMT induction, oncogenic modification of the tumor microenvironment, and enhancing of CSCs self-renewal and differentiation [41], as well as evidence implicating high ERK1/2 activity in the acquisition and maintenance of SOX2-expressing Glioma stem cells [42]. The gene discussed is SOX2; the disease is neoplasm.