We therefore speculate that the release of multiple inflammatory cytokines hindered the generation of ADAMTS13 from stellate cells, endothelial cells, and platelets, leading to secondary TTP-like microcirculatory impairment resulting in PF, although we cannot exclude a possible subclinical heterogenous ADAMTS13 mutation. Here, ADAMTS13 is linked to thrombotic thrombocytopenic purpura.