Furthermore, while we show that the mere presence of the characteristic IgH/c-myc translocation does not suffice to escape CD4 + T-cell-mediated killing in vitro, the CD4 + T-cell-mediated suppression of the Latency III program in vivo may allow cells harboring the IgH/c-myc translocation and additional mutations, to evade immune suppression and eventually proliferate by means of deregulated c-myc activity, resulting in neoplasia. This evidence concerns the gene MYC and neoplasm.