STING1 and neoplasm: The main rationale being that tumors exhibiting HRD have an increased tumor mutational burden leading to higher neo-antigen levels, which increase the anti-tumor immune response.53 Second, PARP inhibition upregulates PD-L1 expression, and in the absence of a functional BRCA pathway there is activation of the innate immune response via the STING/gas pathway.54 The role of the addition of PARPi to immunotherapy was investigated in the DUO-E and RUBY part II studies.