Sunitinib was chosen for several reasons: (1) The NSTS-47 cell line harbors a c.1681C>T (p.R561C) mutation in PDGFRB, and PDGFR-beta was substantially phosphorylated in these cells; (2) sunitinib treatment inhibits PDGFR-beta phosphorylation [25]; and (3) sunitinib was successfully used to treat the boy with IM whose tumor tissue was used to generate the NSTS-47 cell line [8]. Here, PDGFRB is linked to neoplasm.