Further study indicated that PYCR1 deficiency increased PI3K, IRS-1 and p-IRS-1 expression but decreased mTOR expression in HepG2 cells without PYCR1 expression; in addition, PYCR1 deficiency improved insulin resistance mediated by combined glucose/0.5 Gy treatment due to increases in p-Akt, IRS-1 and p-IRS-1 but a decrease in mTOR compared with the levels in HepG2 cells treated with glucose and 0.5 Gy without PYCR1 deficiency (Fig. 8c, d). The gene discussed is AKT1; the disease is Insulin resistance.