Our in vivo experiments indicated that a CSH3-terminally truncated protein that leads to the concurrent hyperstimulation of the RAC1 and NFAT pathways as well as the NOTCH1-derived signals is able to autonomously drive PTCL-like lymphomas in mice, specifically angioimmunoblastic T-cell lymphoma (AITL) subtype (J.R.-V., submitted paper) (Figure 2B). The gene discussed is RAC1; the disease is angioimmunoblastic T-cell lymphoma.