It is D816V, the often occurred KIT mutant in mastocytosis, but not the wild-type KIT, that can phosphorylate PIK3CD, SLAP, MITF and Xkr5, and phosphorylation of these molecules regulates KIT mutations mediated signal transduction and cell transformation in a way that is different from wild-type of KIT [27, 29–31], suggesting that KIT mutants have the activity that wild-type counterpart does not have. Here, KIT is linked to mastocytosis.