On the other hand, silencing ATG4B or overexpressing an ATG4B catalytic mutant (ATG4BC74A) increased adenosine monophosphate (AMP)-activated protein kinase (AMPK) phosphorylation, inactivated mammalian target of rapamycin complex (MTORC), and induced p27kip1 accumulation leading to cell cycle arrest in the G1 phase in colorectal cancer cells [12]. This evidence concerns the gene CDKN1B and colorectal cancer.