Specifically, TRIM59-deleted breast cancer cells favor the amoeboid mode through (i) augmented activation of actomyosin contractile proteins MLC2 and ERM, (ii) excessive formation of E-cadherin-mediated focal adhesion [56], and (iii) the suppression of metastasis-associated Wnt/β-catenin signaling [32–35]. This evidence concerns the gene TRIM59 and breast cancer.