CYP4F3 and acute kidney injury: Later studies showed that AAP can induce renal tubular damage and acute renal failure in the absence of liver injury by a mechanism related to NAPQI production through cytochrome P-450 activation and glutathione depletion, which would lead to NAPQI binding to cellular proteins [44]–[47], despite the low levels of AAP-glutathione conjugate found in kidney by Fisher and co-workers.