Natural in situ activation of DCs could result from damage‐associated molecular patterns (DAMPs) released by tumor cells following immunogenic cell death,61 activation of the cGAS‐cGAMP‐STING pathway by cytosolic DNA,62 complexes of self‐DNA/RNA with cathelicidin (LL37)63, 64 or mitochondrial DNA65 as uncovered for pDCs, or from soluble factors released by tumors cells such as alarmin IL‐33 which was shown to affect DC maturation.66 The gene discussed is IL33; the disease is neoplasm.