We observed that in the high expression groups of RHBDF2 (Figure 2B) and TNFRSF10B (Figure 2C), oxidative phosphorylation was inhibited, while hallmark biological functions such as apoptosis, hypoxia, TNFα signaling via NF-κB, P53 pathway, TGF-β signaling, IL6-JAK-STAT3 signaling, and inflammatory response were upregulated, aligning with changes seen in AD (Figure 2A). This evidence concerns the gene IL6 and Alzheimer disease.