Docking analysisperformed on HDAC3 reported a monodentate Zn2+ chelation,where the NH adjacent to the carbonyl group of thehydrazide chelates with the catalytic Zn2+ through a saltbridge, while the other amino group forms a hydrogen bond with theGly143 residue. Considering the roleplayed by HDAC3 in modulating PD-L1 expression in cancer, compound 11 was assayed on B16–F10melanoma cancer cells, a PD-L1-overexpressing cancer cell line, and a reduced PD-L1 expression was highlighted,thus confirming the HDAC3-driven compound 11’smode of action. The gene discussed is CD274; the disease is cancer.