In summary, our data show that increased SAE1/UBA2 promotes SUMOylation and sequential phosphorylation of PKM2, resulting in a reduction in PK activity, promotion of the nuclear translocation of PKM2, and an increase in STAT5A expression, thereby shunting glucose from oxidative phosphorylation metabolism to glycolysis and promoting aggressive and inflammatory actions in RA FLSs (Figure 7F). The gene discussed is STAT5A; the disease is rheumatoid arthritis.