Previous research found that abnormal activation of the PI3K/AKT signaling pathway by upregulation of CDKs and downregulation of p27Kip1 and p21WAF1/CIP1 increased the proliferation of T lymphocytes might participate in the pathogenesis of SLE in SLE patients (Tang et al., 2009). The gene discussed is CDKN1B; the disease is systemic lupus erythematosus.