Single-cell multi-omics platforms that integrate transcriptomic profiles, T cell receptor repertoires, surface protein expression and, in some cases, epigenomic information can resolve multiple CD8+ T cell states along the continuum from effector to terminally exhausted phenotypes, quantify clonal expansion and lineage relationships, and link these states to clinical trajectories and organ dysfunction in sepsis [25,26,27]. The gene discussed is CD8A; the disease is Sepsis.