The major findings of the study were as follows: (1) PCAF and HDACs regulate the acetylation status of δ-catenin; (2) acetylated δ-catenin is degraded through the Atg5/LC3-mediated autophagosomal pathway; (3) multiple Lys residues in the N-terminus of δ-catenin are involved in PCAF-mediated δ-catenin acetylation; (4) PCAF-mediated δ-catenin degradation decreases the growth and motility of prostate cancer cells; and (5) PCAF-mediated δ-catenin degradation inhibits E-cadherin processing and inactivates β-catenin-mediated signaling. Here, KAT2B is linked to prostate cancer.