A study by Ren F’s demonstrated that psoriasis-like inflammation activated TLR receptors, upregulated the expression of TLR2 and TLR4, activated MyD88 receptor and NF-κB pathway, increased the expression of NF-κB p65, IL-1β, IL-6, TNF-α, and other factors, causing podocytes injury (Ren et al., 2020). The gene discussed is NFKB1; the disease is psoriasis.