The SnMP‐mediated HO1‐inhibition in myeloid cells induces an anti‐tumor immune response via CD8+ T cell adaptive immune responses,[17] and the therapeutic effects of HO1‐inhibiting T‐hNP should be evaluated in an AML patient‐derived xenograft model bearing a human immune system.[38] As described before,[17] HO1 is an enzyme breaking down dying cell released heme, consequently producing biliverdin, Fe2+ and carbon monoxide (CO). The gene discussed is CD8A; the disease is acute myeloid leukemia.