While there was no association between MYCN amplification status and sensitivity to Almac4 (Figure 2D), all sensitive NB cell lines were TP53 wild-type, whereas all resistant cell lines were TP53 mutant or TP53-null, suggesting that p53 status is an important contributor to the efficacy of USP7 inhibition in NB cells and confirming prior results demonstrating the ability of USP7 inhibitors to induce p53-dependent apoptosis in TP53 wild-type NB cells [12]. This evidence concerns the gene USP7 and neuroblastoma.