Subsequently, the team successively found that CD30 could cause DNA double-strand breaks (DSB) by upregulating the levels of intracellular reactive oxygen species (ROS) in ATL and cHL cells, thereby inducing chromosomal instability and clonal expansion (Figure 1), and with the progression of the disease, the amount of copy number loss of genes related to DSB repair would gradually increase (63, 64). This evidence concerns the gene TNFRSF8 and classic Hodgkin lymphoma.