To test this model‐derived hypothesis in primary human hepatocytes, we first investigated the patient‐to‐patient variability in the abundance of the feedback proteins STAT1, STAT2, IRF9, and USP18 by quantitative immunoblotting in patient‐derived primary human hepatocytes that were isolated from tumor‐free tissue of six patients (black bars in Fig 6B). The gene discussed is USP18; the disease is neoplasm.