These findings resemble observations made in IkkbΔhep mice, in which HCC development was suppressed by NAC, a GSH precursor.8 Quantitative reverse-transcription PCR (qRT-PCR) analysis of MUP-uPA/Atf4Δhep livers showed increased expression of F4/80, IL-1α, and C-X-C motif chemokine ligand 2 (CXCL2) mRNAs (Fig. S1G), indicating that ATF4-deficient hepatocytes are more susceptible to ER stress-related necroinflammatory injury, normally suppressed by ATF4, which plays an important role in maintaining redox homoeostasis. The gene discussed is IL1A; the disease is hepatocellular carcinoma.