Overall, our results suggest that PLCη2 and PLCη2_C2 inhibited the proliferation and inflammatory responses of FLSs (which might be closely related to RA-associated intracellular signaling pathways) and that a functional link between PLCη2 and the HRAS–RAF1 protein complex may regulate PLCη2 activity in RA pathogenesis by directly inactivating the signaling pathway. Here, RAF1 is linked to rheumatoid arthritis.