In our previous research, the FGF-2 could inhibit excessive ER stress by activating the PI3K/AKT and MEK-ERK1/2 signaling pathways, thereby reducing the apoptosis of renal epithelial cells induced by ischemia-reperfusion injury [45], and Li et al. have also reported that the FGF-2 could inhibit the expression of CHOP in cancer cells induced by TM [46]. This evidence concerns the gene AKT1 and ischemia reperfusion injury.