These observations together with data from a critical systematic review of all cases of mastocytosis treated with imatinib published in the literature by that time (n=121) support that response to imatinib in SM patients heavily relies on the presence of imatinib-sensitive mutations either involving KIT (e.g. juxtamembrane or transmembrane KIT mutations) or PDGFR (e.g. FIP1L1/PDGFRα rearrangement) rather than on the absence of the D816V KIT mutation (Alvarez-Twose et al., 2017). Here, KIT is linked to mastocytosis.