The efficacy of this combination could be explained not only by an additive antitumor effect but also by the remodeling of the immuno-suppressive tumor microenvironment to an immuno-stimulatory state by inhibiting VEGF.20,21 We could also hypothesize an effect through the KIT pathway, targeted by lenvatinib,22,23 but we need further investigations to better understand the mechanisms involved in mucosal melanoma pathogenesis. Here, KIT is linked to neoplasm.