It has been demonstrated that in lupus‐prone animals, the hypoxic environment linked to renal tissue damage causes CD4+ and CD8+ T lymphocytes to overexpress hypoxia‐inducible factor‐1 (HIF‐1), which leads to metabolic reprogramming, enhanced effector function and resistance to apoptosis. This evidence concerns the gene CD4 and systemic lupus erythematosus.