However, our data showing lack of antitumor effect of TQ in S100A9 KO mice suggest that blocking S100A9 interaction with its receptors may represent the main mechanism by which TQ mediates its effect in vivo. Nevertheless, evaluation of HDAC4 function in multiple myeloma–bearing WT and S100A9 KO mice during disease progression as well as in vitro studies demonstrating dose-dependent response to TQ would contribute to better understanding the role of S100A8/S100A9 proteins in multiple myeloma biology. The gene discussed is HDAC4; the disease is AL amyloidosis.