It provides a mechanistic explanation for the observed clinical phenotypes, showing a particularly poor patient outcome under conditions of high-level PCF11 expression, predominant expression of short TREND isoforms of a neurodifferentiation operon (including AES, IGF1R and GNB1), followed by downstream aberrations of WNT signalling and defective terminal differentiation of neuroblastomas. Here, TLE5 is linked to neuroblastoma.