This may have been caused by different posttranslational modifications (PTMs) of CCL2 (discussed in Can CCL2 Inhibit Tumor Cell Growth and Enhance Tumor Cell Killing by Myeloid Cells?), the presence of other factors in the tumor cell supernatant that suppressed IL-12 production, or the presence of bacteria-derived contaminants (discussed in Considerations Regarding CCL2's Impact on Myeloid Cells), which can be present in recombinant protein preparations and can cause IL-12 stimulatory effects (220, 221). Here, CCL2 is linked to neoplasm.