It was also speculated that its tumor-suppressive function in HCC would probably rely on suppressing CCNE1 expression[11], targeting ZEB2[8], HN1[7], Sox5[41], or ZEB2[42], provoking acetylcholinesterase-independent apoptosis[43], or mediating methylation-silencing and anti-metastasis in the controlling cellular adhesion of prostate cancer [13], which were established by researches on molecular mechanisms of miR-132 as a tumor suppressor in other malignancies. Here, ACHE is linked to neoplasm.