Both p53-dependent and p53-independent mechanisms increase apoptosis; cell cycle arrest triggers p38 and ROS signaling; NF-κB is a tumor-suppressing protein. The peroxisome proliferator-activated receptor (PPAR) activation pathway has improved, as has PPAR activity; phosphorylation of Akt, 4E-BP1, eIF4E, S6R, and p70S6K has decreased. The gene discussed is AKT1; the disease is neoplasm.