In that study, HDAC3 inhibition led to the acetylation of histone H3 at the promoter region of the gene encoding the nuclear ERK1/2 phosphatase, dual specificity phosphatase 5 (DUSP5), preventing diabetes-associated DUSP5 downregulation, which the authors speculated was responsible for ERK1/2-driven cardiac dysfunction in diabetes [120]. The gene discussed is HDAC3; the disease is diabetes mellitus.