Our present study shows for the first time that Aspirin inhibits HDAC6 leading to increased acetylation and phosphorylation of β-catenin and hence decreased FMOD expression and BCCMI, i.e. HDAC6 is a direct target of Aspirin action that mediates the inhibitory effects of Aspirin on the Wnt/β-catenin pathway, and consequently on downstream FMOD, ERK and eventually cell migration and invasion in breast cancer, which identifies HDAC6 as a new target molecule of Aspirin action. The gene discussed is FMOD; the disease is breast carcinoma.