NR4A1 binds and inactivates p53 [35], whereas knockdown of NR4A1, or treatment of p53 wild-type (WT) lung cancer cells with an NR4A1 antagonist or transfection with siNR4A1, result in the activation of p53 and induction of sestrin1 and sestrin2 that activate AMPK and inhibit the mTOR pathway [15]. This evidence concerns the gene MTOR and lung cancer.