In our model, SA14 is internalised through ligation to cell surface receptors, interacts with STAT3, induces its proteasome‐mediated degradation, and suppresses STAT3‐mediated CD274 expression, causing ablation of CSC‐like phenotypes and stimulation of CD8+ T‐cell‐mediated cytotoxicity, which ultimately restores chemosensitivity and suppresses tumour growth (Figure 7J‐i). The gene discussed is CD8A; the disease is neoplasm.