The results of Boisvilliers et al. [78] especially strengthen this potential in the case of retinoblastoma (even in its rare form, where retinoblastoma develops in the absence of an RB1 mutation as a consequence of the somatic amplification of the MYCN gene), as they found that these peptide analogs are capable of inducing a sustained decrease in n-MYC expression and hold potential not only for neuroblastoma therapy but also for addressing other tumors. Here, MYCN is linked to retinoblastoma.