Nevertheless, we believe our findings are of clinical relevance in PTCL as a number of mutated genes, including RHOA, CD28, LCK, FYN, PDK1, PIC3CA, PIK3R1, AKT1 [6, 7, 13, 53], as well as the fusion proteins NPM-ALK and ITK-SYK [4, 5, 26, 54, 55] either are part of, or can activate, the TcR/PI3K/AKT signaling pathway and our prediction is therefore that expression of at least some of these mutated genes would have the ability to substitute for activated AKT in the experimental system described herein. This evidence concerns the gene ALK and mature T-cell and NK-cell non-Hodgkin lymphoma.