First, pharmacological inhibition or genetic inhibition of BCL2 in de-iniDCs (which transcriptionally and functionally resemble cDC1 cells and can functionally reconstitute cDC1-deficient Batf3-/- mice with respect to cancer immunosurveillance) enhances their antigen-presenting function, induces a marked type-1 interferon response and upregulates DC activation markers in vitro. The gene discussed is BCL2; the disease is cancer.