STAT3 and neoplasm: This immunodeficiency is exacerbated by “inflammaging,” a chronic, low-grade inflammatory milieu typified by raised IL-6, TNF-α, C-reactive protein and HMGB1, which drive STAT3-and NF-κB-mediated proliferation, angiogenesis, epithelial–mesenchymal transition and recruitment of suppressive myeloid and regulatory cells, thereby re-shaping the tumour microenvironment toward immune evasion (Li et al., 2024).