CSE increased expression of EZH2 and methylation of histone H3; epigenetic silencing of pre-miR-218 downregulation by EZH2 was discovered to be the molecular mechanism allowing increased expression of BMI1, whereas overexpression of miR-218 resulted in loss of cancer stemness properties and decrease of migration and invasion in cells treated with CSE. The gene discussed is EZH2; the disease is cancer.