This finding contradicts in vitro results where MGMT expression (e.g. unmethylated status) leads to altered expression of receptor tyrosine kinases and significant inhibition of cell proliferation by the addition of sunitinib to the combination of TMZ and/or radiotherapy.49 These preclinical findings led to a phase II trial where sunitinib was added to standard first-line therapy in recurrent glioblastoma patients with unmethylated MGMT. The gene discussed is MGMT; the disease is glioblastoma.