By comparing upregulated DEGs regarding C08 versus C10, it further substantiated the dysfunctional phenotype of HLA-DRlowS100Ahigh monocytes, as shown by dampened expression of functional molecules and significant upregulation of damage-associated molecular patterns, including S100A family genes and LGALS1, which greatly prompted programmed cell death and immune disorder (Fig. 2d). This evidence concerns the gene LGALS1 and immune system disorder.