PPARGC1A and thyroid gland carcinoma: Akt also promotes glucose uptake through both GLUT1 and GLUT4, then activation of specific glycolytic enzymes in glycolysis.43,44 In thyroid cancer, PGC1α knockdown was inversely related to AKT activity, induced a glycolytic phenotype and suppressed tumor growth.17 However, the expression of PI3K and Akt mRNA/protein level is decreased in shPGC1α cell in our study, and the glycolysis enzymes (HK1/2, PKM, LDHA), GLUT1/3/4, glucose uptake is higher, which indicted that PI3K/Akt signaling pathway not involved in regulating glycolysis.