Specifically, Fugazzola et al. revealed that the expression of three inflammation-related genes (CCL20, CXCL8 and l-selectin) was enhanced in BRAFV600E and in RET/PTC tumors, as compared to normal samples: this resulted in a reciprocal interaction among tumor cells, stromal cells and all the other TME components, actively fostering an inflamed, pro-tumorigenic microenvironment [14]. The gene discussed is CCL20; the disease is neoplasm.