H. pylori Vac-A has a variety of cellular actions, including the utilization of cellular vacuoles to increase the lifespan of infection, as well as mitochondrial stress, and interference with apoptosis (53), Vac-A also regulates host cell metabolism, stimulating all three of these pathways, including NFE2L2 / HO-1 /Nrf2-HMOX1, through the dependent inhibition of MTORC1 (54). Here, HMOX1 is linked to infection.