KIT and systemic mastocytosis: Similarly to SM patients, the presence of activating KIT mutations in clonal MCAS results into a constitutive, ligand-independent hyperactivation of the KIT receptor; this eventually induces the activation of several intracellular downstream signaling pathways involved in differentiation, maturation, migration, activation, and survival of MCs, such as the Ras, Jak, and phosphatidylinositol 3-kinase (PI3K) pathways (17).