Clearly, any potentiation of YY1-induced AANAT, if coupled to AhR-induced CYP1B1 and the NAS activation of the BDNF receptor, TrkB, could allow co-ordinated O-GlcNAcylation to provide trophic support to tumours, whilst protecting mitochondria, limiting OXPHOS, maintaining HIF-1α and upregulating PFK1, PGK1 [121] and therefore glycolysis and the pentose phosphate pathway [110]. The gene discussed is CYP1B1; the disease is neoplasm.