HSF1 knockdown in sphere-forming human A172 glioblastoma CSCs resulted in failing of the spheroid-forming capacity, reduced expression of SOX2 (a marker of stemness), and downregulation of MMP2 activity; such an addiction of the glioblastoma CSC phenotype to HSF1 was somehow supported the Bcl-2-interacting cell death suppressor (BIS), as BIS depletion led to a decrease in the HSF1 protein level [168]. Here, BCL2 is linked to glioblastoma.