The present work also demonstrates at the molecular level that QLY as a Cold-natured formula is likely to modulate these network hub molecules of Hot syndrome (IL1B, TNF, and VEGF), aiming to expel the “pathogenetic hot” for curing Hot syndrome-related RA and exert the antiangiogenesis, anti-inflammation, and immune-regulatory actions (Figure 4 and Table 1). Here, TNF is linked to rheumatoid arthritis.