While combined inhibition of HDAC3 and HDAC6 (by RGFP-966 and tubastatin, respectively) attenuates LPS-induced ALI in mice [118], a recent study demonstrated that MS-275 compound (entinostat), inhibits HDAC1, HDAC2, and HDAC3 activities [254], suppresses Robo4 expression by inhibiting HDAC3 in ECs and enhances EC permeability and lung vascular leakage in mice [110]. The gene discussed is HDAC2; the disease is acute respiratory distress syndrome.