The authors found that the epitope encoded by the SLE-risk allele DRB1*03:01, the most significant genetic risk factor for SLE [92], activated a SLE transcriptome and triggered a cascade of SLE-associated cellular aberrations, including production of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), activation of proteasomal degradation and UPR pathways, reduction of intracellular ATP levels, loss of mitochondrial membrane potential, increase in mitochondrial superoxide production, and cell death by necroptosis; all of which were mitigated with 4-PBA treatment. This evidence concerns the gene TNF and systemic lupus erythematosus.