The secreted IL-6 subsequently activates the JAK–STAT3 cascade in tumour and immune cells, driving a series of tumour progression-associated phenotypes, including the upregulation of proliferation and anti-apoptotic programmes (e.g., target genes such as BCL-XL and Survivin), the maintenance of the inflammatory microenvironment (by synergising with TAM/MDSC polarisation) and the development of chemotherapy tolerance (preclinical evidence supports its role in promoting docetaxel resistance) (Matsushita et al., 2022; Shan et al., 2025). This evidence concerns the gene STAT3 and neoplasm.