Additionally, ellagic acid-binding to LOXL2’s catalytic domain results in a metabolite byproduct that also inhibits TGF-β receptor I31, imparting a secondary effect that reduces TGF-β-induced collagen production by cancer cells and prevents TGF-β recruitment and maintenance of regulatory T cells that are responsible for tumor immune suppression62. This evidence concerns the gene LOXL2 and neoplasm.