The contrasting responses to arginine depletion, demonstrating enhanced IFNγ-JAK-STAT activation with limited tumor growth inhibition in vivo, versus suppressed IFNγ signaling and heightened sensitivity in vitro, suggest that IFNγ signaling in cancer cells may be a compensatory rescue mechanism induced by the cross-talk between cancer cells and other cells in the TME to support tumor cell survival under arginine-deprived conditions. The gene discussed is SOAT1; the disease is cancer.