GLI1 and neoplasm: Among the majority of the colorectal tumors that exhibited no mutational evidence of mismatch repair deficiency, two harbored homozygous deletions in SUFU, one of which occurred in a tumor that had also amplified GLI1. The latter tumor exhibited elevated GLI1 expression (approximately one standard deviation above the mean); the tumor harboring only the SUFU deletion did not exhibit elevated GLI1 expression (Fig. panel A).