Later, a possible explanation was suggested by the disclosure of the butyrate molecular mechanism which comprises the following: (a) activation of the G protein-coupled receptor 109a (GPR109a)–AKT signalling pathway, which leads to the remarkable inhibition of glucose metabolism and DNA synthesis in CRC cells, via reducing the amount of membrane G6PD and GLUT1 [163]; (b) the inhibition of AKT/ERK signalling in a histone deacetylase (HDAC)-dependent manner [164]. The gene discussed is HCAR2; the disease is colorectal carcinoma.