Efficacy of current anti‐GD2 immunotherapy in 11q‐deleted neuroblastomas may be reduced by inhibition of effector cells by kynurenine production and tryptophan depletion by IDO1, polarized M2 macrophages, PD‐L1 expression, and IL‐10‐dependent Treg conversion from resting CD4+ T cells, providing a rationale for further combination immunotherapy studies. The gene discussed is CD4; the disease is neuroblastoma.