Importantly, previous studies have confirmed modest response rates to temozolomide given as a single agent in colorectal cancers with MGMT promoter methylation (26, 27), and to temozolomide-based regimens in pancreatic neuroendocrine tumors lacking MGMT protein expression (28), supporting our observations that MGMT deficiency may be a predictor of response to temozolomide regardless of tumor histology. This evidence concerns the gene MGMT and colorectal cancer.