Given that the PD‐1/PD‐L1 axis accelerates tumor growth mainly by repressing the antitumor killing activity of T cells in the TME and that PD‐L1 was down‐regulated upon EHBP1L1 loss, we depleted CD4+ T cells, CD8+ T cells, or both to further validate whether T cell populations contribute to the improved antitumor immunity upon EHBP1L1 loss. The gene discussed is CD4; the disease is neoplasm.