HK2 and arthritic joint disease: These results, together with the mRNA expression profile and the intracellular metabolomic profiles, indicate that both the glycolytic and glutaminolytic pathways are upregulated in RA-FLS, and are consistent with previous reports showing that the inhibition of HK2, MCT4, or PDK1 suppresses RA-FLS proliferation and arthritis in a mouse model [22, 24, 26].