Conversely, upstream components of the mTOR pathway are frequently altered in human tumours (8,15), and UBC is not an exception, with reported mutations of phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha, AKT1 and tuberous sclerosis protein 1, hamartin, and loss of heterozygosity, homozygous deletion and inactivating mutations of phosphatase and tensin homologue deleted on chromosome 10 (39,40). Here, MTOR is linked to neoplasm.