We also found that a PI3Kγ inhibitor combined with anti‐PD‐1 therapy can enhance the antitumor effects of anti‐PD‐1 agents by modulating the PI3Kγ‐AKT‐NF‐κB pathway, reprogramming TAMs, decreasing the number of myeloid‐derived suppressor cells, increasing the number of CD8+ T cells, and increasing the levels of proinflammatory factors; consequently, this approach transforms the tumor immune microenvironment of OC into a more active state. Here, NFKB1 is linked to neoplasm.