Tumours which utilise acetate as a carbon source also show elevated activity of ACSS2. Mutations causing PTEN and BRAF inactivation driving AKT and ERK pathways have been found to play role in increased expression of ACSS2. Tumours devoid of this enzyme consume less amount of acetate, undergo cell death, and subsequently reach to a reduced tumour size (86). Here, BRAF is linked to neoplasm.