These efforts have yielded an emerging understanding of the dysregulating alterations in 3 key molecular signaling pathways, namely receptor tyrosine kinase/phosphoinositide 3-kinase (RTK/PI3K), p53, and Rb, as obligatory events in GBM tumorigenesis.5,6 Further gene expression–based molecular studies have facilitated tumor classification into clinically relevant subtypes that may exhibit distinct treatment response characteristics.7 The gene discussed is NTRK1; the disease is glioblastoma.