Almost parallel studies also showed that HDAC6-selectiveinhibition through the use of TubA promoted bacterial clearance, reducedpro-inflammatory cytokine production, restored innate immune cellpopulations in the bone marrow, and improved survival in a mouse modelof sepsis (Figure 6).128,129 These data, together with the evidence linkingHDAC6 to control of mitochondrial function and stimulation of mitochondrialROS production, suggest a crucial role for HDAC6 in regulating bacterialclearance,130−132 while class I HDACs seem unlikely to exertsuch an effect. The gene discussed is HDAC6; the disease is Sepsis.