On one hand, LILRB3 may promote tumor cell proliferation and metastasis by activating the PI3K/AKT/mTOR signaling pathway; on the other hand, the upregulation of PD-L1 expression by LILRB3 might contribute to establishing an immunosuppressive tumor microenvironment, enabling tumor cells to evade immune recognition and clearance, thereby facilitating further tumor progression and deterioration.These findings indicate that LILRB3 plays a pivotal role in the functionality of ccRCC cells, and modulating its expression levels may represent a potential therapeutic strategy for ccRCC. Here, AKT1 is linked to neoplasm.