This is associated with a lack of repression of its target genes [28], which can lead to processes that enhance neoplastic activity, such as increased proliferation through its interaction with STMN1 [29], epithelial–mesenchymal transition via its interaction with CDH2 [30], changes in cellular phenotype due to the re-expression of neuronal genes like SCN1 or BDNF [31,32], and the survival of tumor cells through the expression of GRIA1 and GRIA2, which encode glutamate receptors involved in synaptic signaling [33]. The gene discussed is CDH2; the disease is neoplasm.