Emerging data reported that during bacterial infection associated with decompensated cirrhosis, certain types of monocytes, known as monocytic myeloid-derived suppressor cells (M-MDSCs) and MER-receptor tyrosine kinase (MERTK) cells, migrate to the infection site impairing the potential activation of T cells; indeed, the phenotype of effector CD8+ T cells changes into the exhausted one, which is characterized by increased expression of programmed cell death protein 1 (PD-1) and T cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) [17,18]. This evidence concerns the gene HAVCR2 and infection.