In vitro experiments indicated that 4-PBA treatment inhibited macrophage attachment to human aortic endothelial cells, prevented ER stress-induced cell death, increased the nuclear localization of HSF1 and the expression of HSP27, and may have exerted a therapeutic effect on atherosclerosis through this pathway; however, the exact mechanism needs to be investigated further (107). The gene discussed is HSPB1; the disease is atherosclerosis.