“…Several somatic mutations of c- kit have been implicated in various malignancies, including mastocytosis [10]. Upon activation, MCs can release a plethora of mediators, which includes: preformed mediators stored in their cytoplasmic granules, such as histamine, tryptase and other proteases, cytokines [tumor necrosis factor-α (TNF-α), fibroblast growth factor (FGF), IL-4 and SCF] and proteoglycans (heparin, chondroitin sulfates) [10,15]; neoformed or lipid mediators, products of phospholipase A 2 activation, such as prostaglandins, leukotrienes and platelet-activating factor [4,10,16], and neosynthesized mediators, produced and released upon transcriptional activation, such as IL-1, IL-5, IL-6, IL-8, IL-9, IL-13, IL-17, TNF-α, transforming growth factor-β, FGF and vascular endothelial growth factor (VEGF) [4,10,17,18,19]. …”