We can determine that human sPLA2s released in the TME by tumor cells, stromal cells or other inflammatory cells infiltrating the tumor (e.g., mast cells and neutrophils) could act as a driving stimulus activating TAMs to produce cytokines, chemokines and angiogenic factors, without a clear polarization toward an M1- or M2-like functional output (Figure 2). The gene discussed is PLA2G2D; the disease is neoplasm.