When in the TME, such polarizing stimuli as INF-γ, adenosine or IL-4 produced together with sPLA2s, can polarize the functional output of sPLA2-activated TAMs toward an M1-like (e.g., stimulation of TNF-α plus inhibition of VEGF-A), M2-like (e.g., inhibition of TNF-α plus stimulation of VEGF-A), or anti-inflammatory (e.g., inhibition of TNF-α and VEGF-A) phenotype to modulate tumor growth and progression. This evidence concerns the gene IL4 and neoplasm.