Evidence suggests that HIF‐1α knockdown decreases the expression of PFKP and LDHA, while upregulating enzymes involved in OXPHOS and fatty acid oxidation, indicating that targeting HIF‐1α could effectively shift the metabolic balance from glycolysis back to OXPHOS, thereby reducing RA FLS proliferation [85]. The gene discussed is HIF1A; the disease is rheumatoid arthritis.