The investigation into the potential efficacy of the PD-1-PD-L1 pathway as an inhibitory mechanism in the progression and development of LN in mice, and the search for a potential efficient treatment approach for SLE [57]. Significant to the pathogenesis of SLE, two critical signaling pathways, type I interferon and toll-like receptor, influence the expression of PD-1 and its ligands (PD-L1, PD-L2) via activation of NF-κB and/or STAT1 [58]. The gene discussed is STAT1; the disease is lobular neoplasia.