GLI1 and acute lymphoblastic leukemia: Additionally, the same group reported that the HH cascade was active in ≈20% of the patient samples, through ectopic expression of SHH and IHH and of the downstream GLI1 transcription factor, suggesting that the crosstalk with other pathways such as IL-7, vascular endothelial growth factor (VEGF) or NOTCH signaling pathways and the overall transcriptional deregulation intrinsic to T-ALL, rather than pathway-intrinsic mutational events, are responsible for this activation [197].