Acetaminophen overdose is still a major cause of liver toxicity (acute liver failure, ALI) in Western countries. It occurs by accumulation of the toxic metabolite NAPQI and the subsequent mitochondrial oxidative stress mediated by pJNK translocation to the mitochondria.

An international study led by scientists at Duke-NUS Medical School in Singapore has identified signaling for the cytokine IL-11 as representing a potential new therapeutic target for acetaminophen-induced liver injury in mouse models.