Under persistent inflammatory stimuli (e.g., MTB infection combined with hyperglycemia), sustained NF-κB/MAPK hyperactivation may trigger negative feedback mechanisms [40], such as upregulating inhibitory receptors (e.g., PD-1 and CTLA-4) or Tregs, thereby suppressing effector T-cell function. This evidence concerns the gene NFKB1 and Hyperglycemia.