The landscape of CNAs and SVs revealed potentially clinically exploitable deletion of TOX as a predictor for anti-PD1 response103, amplification of MALT1, whose inhibition has been shown to be selectively toxic for ABC-DLBCL151, and potential enhancer-hijacking events involving PIK3C3 and EPHA4, whose inhibition has shown therapeutic advantage in a number of cancer models113–115,120. The gene discussed is TOX; the disease is cancer.