It showed that UTI (1)improves neurological dysfunction after ICH, (2) alleviates brain damage in a mouseICH model, (3) relieves neuroinflammation after ICH and then decreases inflammatorydamage in the brain, and (4) prevents necroptosis after ICH and alleviates neuronaldeath; (5) the antinecroptosis and antineuroinflammation effects of UTI may berelated to the MAPK/NF-κB signaling pathway (Fig.7). This evidence concerns the gene NFKB1 and bacterial urinary tract infection.