The autophagy inhibitor 3-MA and lysosome inhibitor CQ failed to alter the protein level of OX-42 after CCH, while the microglial activation inhibitor minocycline could reverse the CCH-induced protein levels of LC3, p62 and LAMP1, suggesting that microglial overactivation may be the upstream regulator of autophagy after CCH. This evidence concerns the gene MAP1LC3A and columnar cell hyperplasia of the breast.