Further investigations should include the following: multidirectional studies on the molecular mechanism of A2M’s inhibition of migration, invasiveness and tumorgenesis, which, according to the current knowledge, is probably related to upregulation of LRP1 and frizzled receptor (FZD); the inhibition of the expression of Wnt ligands and, hence, the autocrine activation of Wnt/β-catenin signalling; and the relocation of beta cathenin and the induction of cellular cadherins, which act as tumor supressors [30]. The gene discussed is LRP1; the disease is neoplasm.