Collectively, in most of the cases, the expression of H3K9 modifiers and effectors is inversely correlated with canonical immune signatures (e.g., IFN, TNFα/NF-κB signaling, inflammatory response, JAK/STAT pathway) and cytolytic features, which characterize immune-excluded tumors (i.e., cold tumors). The gene discussed is SOAT1; the disease is chronic obstructive pulmonary disease.