Since SLE-AH patients had upregulated SNHG16 expression, increased pro-inflammatory cytokine levels and increased apoptosis formation in their lung tissues, we further investigated whether, in alveolar cells, the presence of pro-inflammatory cytokine could regulate the expression of SNHG16, and the apoptotic status could be altered by overexpressing or silencing the expression of SNHG16. The gene discussed is SNHG16; the disease is systemic lupus erythematosus.