An alternative target for treatment of TRK-fusion cancers was identified by Sorensen and co-workers who showed that the ETV6–NTRK3 fusion requires an intact IGF1R–PI3K–AKT axis for neoplastic transformation [69,70], and that IGF1R inhibitors can block ETV6–NTRK3-mediated tumorigenesis in vivo [66,70]. The gene discussed is NTRK3; the disease is cancer.