PCGs mainly participated in an inflammatory response, TNF-α signaling, hypoxia, epithelial-mesenchymal transition (EMT), and interferon-γ response (Figure 4(a)), and was involved in focal adhesion, primary focal segmental glomerulosclerosis, PI3K-AKT signaling pathway, and AGE-RAGE pathway (Figure 4(b)). This evidence concerns the gene TNF and focal segmental glomerulosclerosis.