2019). This dual approach strengthens the relevance of our findings and suggests that BEVs may indeed play a significant role in SLE pathogenesis. Additionally, our exploration of the TLR2‐MyD88‐NF‐κB pathway offers a potential target for therapeutic interventions that could dampen inflammatory responses associated with SLE (Aringer 2020; Dutta et al. 2021; Gallardo‐Zapata et al. 2024). The gene discussed is NFKB1; the disease is systemic lupus erythematosus.