Further, as cancer cell models deficient in ARID1A are more sensitive to ATR inhibition through a synthetic lethality mechanism65, there is a rationale to combine immunotherapy with ATR inhibitors in TMB-high tumours harbouring ARID1A GAs, which is based on data linking ARID1A GAs and TMB-high status to ATR inhibitor and immune checkpoint inhibitor sensitivity, respectively. The gene discussed is ARID1A; the disease is neoplasm.