TCF1+CD8+ T cells exhibit an ‘exhausted’ phenotype, expressing high levels of inhibitory receptors such as PD-1 and Lag-3 in chronic viral infections and tumours [52,53] and are therefore key targets for ICIs, which both mobilise TCF1+CD8+ T cells and activate differentiation into effector T cells for tumour rejection [53–55]. Here, CD8A is linked to neoplasm.