As C‐MYC overexpression and p53 mutations in cancer cells cooperate to induce highly aggressive phenotypes and poor responses to treatment, C‐MYC has become an appealing therapeutic target for developing anticancer drugs especially when p53 is mutated.[4, 33] However, the intrinsically disordered functional domains of C‐MYC and the lack of enzymatically active pockets limit the efficacy of traditional approaches that directly target this oncoprotein. This evidence concerns the gene TP53 and cancer.