In this study, early lesions have shown to bear a unique and TNM stage-independent immune signature, with a particular subset of tumor-infiltrating myeloid cells different from normal lung—PPARγhi macrophages enrichment and CD141+ dendritic cells (DC) depletion)—which could be compromising T cell immunity and may offer a new avenue of intervention in T cell immunotherapies. This evidence concerns the gene THBD and neoplasm.