Although the SM incidence by TRKA activation was lower than by TRKB activation (3/7 = 43% vs. 12/17 = 71% [19]), our data indicate that activation of both TRKA and TRKB by their ligands are more potent than KIT D816V for induction of SM [19], since SM was not induced by retroviral-mediated expression of KIT D816V in similar settings [22]. This evidence concerns the gene NTRK2 and systemic mastocytosis.