T-ALL is marked by the transcriptional activation of several protooncogenes, submicroscopic deletions of cancer suppressor genes, epigenetic deregulation, ribosomal dysfunction, altered RNA stability, cell-cycle dysregulation, and disordered signaling in the pathways NOTCH1/FBXW7, PI3K/Akt/mTOR, RAS/MAPK, and IL7R–JAK–STAT [7,16]. The gene discussed is NOTCH1; the disease is acute lymphoblastic leukemia.