In regard to the possible mechanism by which WD/IL-1β induces TRIM13 expression, our observations revealed that WD and IL-1β triggers activation of Sp1 in vivo in ApoE−/− mice and in vitro in peritoneal macrophages and MASMCs, respectively, and depletion of Sp1 levels attenuate IL-1β-induced TRIM13 expression, it is likely that Sp1 plays a role in WD/IL-1β-induced TRIM13 expression. Here, SP1 is linked to Wilson disease.