EGFR modulates glucose levels in cancer cells by regulating sodium/glucose cotransporter 1 (SGLT1) independent of receptor tyrosine kinase activities [29], and activates SREBP1 and SCD1 through PI3K/Akt pathway [13, 22], indicating that GK5 might allow cancer cells to escape apoptosis promoted by gefitinib treatment by regulating EGFR/PI3K/AKT/SREBP1/SCD1 pathway. This evidence concerns the gene GK5 and cancer.