As this Ab was shown to interfere with HMGB1-mediated induction of proliferation and cytokine production in HaCaT or HEKA cells (see above), our data suggest that HMGB1(+) sEV-induced effects were mediated through phosphorylation of these proteins, and that the effect is much stronger for sEVs isolated from cholesteatoma patients. The gene discussed is HMGB1; the disease is cholesteatoma.