Under the specific intra-pulmonary cytokine milieu with increased IL-6 expression in the SLE-AH lungs, upregulated SNHG16 levels in alveolar cells and resident neutrophils can enhance TLR4 expression via stabilizing its mRNA expression and sponging miRNAs that can target it, e.g. miR-146a [27–29]. The gene discussed is TLR4; the disease is systemic lupus erythematosus.