For example, it promotes gastric cancer metastasis via interaction with Arp2, MMP-9, and cathepsin K (Ren et al., 2012; Sun et al., 2014), increases matrix degradation and invasion and decreases adhesion and formation of invadopodia-like extensions in glioblastoma cells (Ziemann et al., 2013). This evidence concerns the gene CTSK and glioblastoma.