AKT1 and neoplasm: Prostaglandin 15d-PGJ2 produces an increase in ROS through mitochondrial dysfunction, activation of NADPH (Nicotinamide adenine dinucleotide phosphate) oxidase and JNK, and inhibition of AKT, which favors tumor apoptosis through the TRAIL (TNF-related apoptosis-inducing ligand) pathway associated with an increase in the concentration of the DR5 receptor, through a mechanism independent of the PPARγ pathway [36].