A recent report shows that impaired activity of macrophages and the lack of inflammation‐resolving regenerative macrophages at the site of injury disturbs tissue repair in humans suffering from diabetic foot ulcers.[11, 12, 71] Unexpectedly and previously unreported, we here provide evidence that the HDAC inhibitor butyrate is responsible for the reversal and activation of the suppressed acetylated (Lys27 or Lys9) histone mark in diabetic macrophages promoting the beneficial resolution of the persisting ineffective inflammation of wounds in db/db mice. Here, HDAC9 is linked to diabetic foot.