When sepsis samples were compared to healthy it was revealed that the predicted upregulation of coagulation system (p = 7.94 × 10−23), acute phase response signalling (p = 3.98 × 10−19), LXR/RXR activation (p = 2.51 × 10−17), extrinsic and intrinsic prothrombin activation pathways (p = 2 × 10−16 and p = 1 × 10−14), complement system (p = 3.16 × 10−11), neuroprotective role of THOP1 in Alzheimer's disease (p = 1.55 × 10−6) and OA pathway (p = 7.08 × 10−6); and inhibition of matrix metalloproteases was downregulated (p = 2.51 × 10–15) (Fig. 4A). This evidence concerns the gene THOP1 and early-onset autosomal dominant Alzheimer disease.