Important molecular features correlating with the differences in clinical outcome are telomerase activation [10], the status of the MYCN oncogene, which is amplified in about 20% of all NB [11], loss of heterozygosity at chromosomes 1p [12] or 11q [13], trisomy of 17q [14], and high expression of the neurotrophin receptor TrkB/NTRK2 [15], all of which are linked to unfavorable outcome [16]. Here, NTRK2 is linked to neuroblastoma.