Our previous studies revealed that in breast cancers, LMO2 could attenuate the canonical Wnt-β-catenin signal pathway via binding with dishevelled-2 protein in a subtype-independent manner [2], while specifically in basal type breast cancer, LMO2 could promote tumor cell migration, invasion and metastasis via blocking the LIMK1-mediated cofilin1 phosphorylation [17]. This evidence concerns the gene LIMK1 and neoplasm.