Therefore, inhibition of LOX and LOXL with specific molecules such as beta-aminopropionitrile (BAPN), which irreversibly binds to the catalytic domain, or with antibodies directed to the catalytic domain of LOXL2, such as simtuzumab, or by inactivation of bone morphogenetic protein 1 (BMP1), which activates LOX by cleavage, or the use of copper chelators, such as tetrathiomolybdate, which is essential for the activity of the catalytic domain of LOX, has been shown in preclinical studies to improve the anti-tumor response of therapies in several tumor types. Here, LOXL2 is linked to neoplasm.