One possibility is that Gln158 could be resistant to MMP2 proteolytic cleavage at residue 158 which then may alter the activity or substrate specificity of pro-LOX in favor of more BMP1/procollagen C-proteinase cleavage at residue 158, resulting in the formation of active LOX, which is well-known to be upregulated in a variety of cancers [39,40]. This evidence concerns the gene LOX and cancer.