Utilizing a novel gene expression analysis to determine the impact of the differential cortical transcriptomic fabric between Fn14-sufficient and Fn14-depleted lupus-prone mice would allow for the identification of crucial signaling pathways activated by the TWEAK/Fn14 interaction, emphasize relevant neurotransmission processes, and potentially identify new promising therapeutic targets. The gene discussed is TNFRSF12A; the disease is systemic lupus erythematosus.