CD133 silencing reduces proliferation, clonogenic capacity, migration, cell invasion, and resistance in CRC in part through decreasing glucose uptake as a result of the low GLUT1 expression because of impaired HER3/Akt pathway involved in protein synthesis via mTOR and mRNA stability, probably through the regulation of RNA-binding proteins [70, 71]. The gene discussed is PROM1; the disease is colorectal carcinoma.