Another group could demonstrate a non-canonical activation of GLI1 in esophageal adenocarcinoma via TNF-α and subsequently mTOR/S6K1 [21] while Zhou and colleagues could recently show that GLI1 and GLI2 are non-canonically activated via PI3K/AKT in human renal cell carcinoma [9]. This evidence concerns the gene MTOR and hereditary clear cell renal cell carcinoma.