Cluster analysis divides sepsis patients into two groups: Cluster 2 has an increased proportion of plasma B cells, linked to MKI67-driven B cell differentiation, though their hyperactivation or exhaustion may impair immunity (61, 62); Cluster 1 shows increased neutrophil infiltration, associated with activation of the CREB5/SULT1B1-regulated chemokine pathway, whose phagocytic function is coordinately regulated by the FcγR pathway and MYO10/CREB5 (61, 63). This evidence concerns the gene SULT1B1 and Sepsis.