Tissue lysis during hyperacute rejection produces cellular debris that is immune-complexed with anti-Gal IgG and various complement proteins, while complement activation will cause the release of inflammatory mediators such as the anaphylatoxins C3a and C5a, which create an inflammatory tumor microenvironment that is optimal for the chemotactic recruitment and activity of antigen presenting cells (APCs), such as macrophages and dendritic cells (DCs). Here, GAL is linked to neoplasm.