NEK2 is considered a key factor in the maintenance of development and function of B cells in multiple myeloma (MM). Importantly, we previously demonstrated that PD-L1 is a substrate of NEK2, and combinatorial inhibition of NEK2 and PD-L1 largely improves the therapeutic efficacy of pancreatic cancer in pre-clinical models. But the expression and function of NEK2 in HCC-related TAMs have not yet been studied. This analysis revealed changes in the proteome due to the overexpression of NEK2 in TAMs, providing a valuable reference for further functional investigations.