We suggest that loss of GSTZ1‐1 results in the accumulation of the oncometabolite SA, alkylation of KEAP1, and NRF2 activation, promoting IGF1R transcription by recruiting SP1 to its promoter, which promotes the antiapoptotic pathway of hepatoma cells in vitro and in vivo. The gene discussed is IGF1R; the disease is hepatocellular carcinoma.