Therefore, they designed a cancer-selective MDMX-ASO that targets the exon–intron boundary of exon 6 and leads to a reduction in MDMX protein levels, impaired in vitro growth, and increased apoptosis induction as well as attenuated the growth of both melanoma and large B cell lymphoma patient-derived xenografts (Figure 2B). This evidence concerns the gene MDM4 and melanoma.