Constitutively activated NFκB in GBM tumors promotes their growth and survival.14 PPARγ is known to induce proteosomal degradation of NFκB,15 and NFκB regulates CIDEA expression.16 As there was no significant change in expression of NFκB upon PPARγ inhibition (Figure 3a), we determined whether PPARγ inhibition affects DNA-binding pattern of NFκB on CIDEA promoter. Here, CIDEA is linked to glioblastoma.