What we know is that the superior responsiveness to immune checkpoint inhibitors (such as anti-PD-1) is mediated by the reactivity of expanded CD8+ T cells towards the tumor antigens [131,132], especially in tumors with a high mutational burden, with mismatch repair deficiency and a high DNA microsatellite instability, typical of CCA [133,134]. The gene discussed is CD8A; the disease is neoplasm.