The established efficacy of PD1/PD-L1 inhibitors in metastatic RCC [31, 32], coupled with increased anti-tumour activity of immune checkpoint inhibitors in combination with DDRi, owing to the increased expression of PD-L1 and activation of the stimulator of interferon genes (STING) pathway observed pre-clinically, rationalises this combination treatment [33, 34]. The gene discussed is STING1; the disease is neoplasm.