To focus on the Ikaros–SIRT1 axis in BMM activation/recruitment in vivo, we utilized the CD11b-DTR mouse system, in which: i) adoptively transferred Ikaros-proficient BMMs recreated liver damage in otherwise IRI-resistant CD11b-deficient recipients; ii) Ikaros-silenced BMMs ameliorated liver IRI/pyroptosis, compared with Ikaros-proficient controls; and iii) SIRT1 was readily expressed by adoptively transferred liver-infiltrating Ikaros-silenced CD11b+ BMMs. The gene discussed is IKZF1; the disease is medical procedure.