On the one hand, it reduced the upstream driving force of UDP-GlcNAc synthesis (glucose uptake by HK2 and CRC cells), and on the other hand, it enhanced the downstream metabolic flow (GFAT/PGM3), which ultimately led to a reduction in the cellular UDP-GlcNAc pool, further limiting the availability of OGT substrates. The gene discussed is OGT; the disease is colorectal carcinoma.