It is known that the phosphorylated form of AKT can promote MDR by: (i) stimulating induced myeloid leukemia cell differentiation protein (MCL-1) that promotes EMT in lung cancer cells [39]; (ii) triggering phosphorylation of anti-apoptotic mouse double minute 2 homolog (MDM2), which inhibits activation of the intrinsic apoptotic pathway; (iii) inducing the phosphorylation of oncogenic mTOR, responsible for autophagy inhibition; and/or (iv) increasing the expression levels of cellular inhibitor of apoptosis protein-1 and -2 (cIAP-1/2) through nuclear factor NF-κB. This evidence concerns the gene MTOR and lung cancer.