To experimentally dissect the potential link between the ability of NACT to alter the immunological configuration of the metastatic HGSOC microenvironment in patients, we harnessed two mouse models of ovarian cancer that exhibit significantly different tumor mutational burden (TMB), namely, ID8 cells and Brca1−/−Trp53−/−/Myc/Hras SO1 cells to establish progressive intraperitoneal disease in immunocompetent syngeneic hosts and test the therapeutic efficacy of carboplatin-paclitaxel doublet chemotherapy optionally combined with ICIs (Fig. 6A–C). The gene discussed is HRAS; the disease is ovarian cancer.