These conventional CTLs typically recognise tumours with a high tumour mutational burden due to the ability of their TCRs to detected mutated neoantigens as “non-self”.4 In contrast, elegant TCR reporter assays demonstrated that the majority of the TCRs from NK1.1+CD8α+ αβILTCKs showed reactivity against unmuted antigens from heterologous cancer cell populations.1 In this setting, the αβILTCK derived TCRs recognise the cancer-specific peptide in the context of major histocompatibility complex class I (MHC-I) complexes. The gene discussed is CD8A; the disease is neoplasm.