Moreover, it has been revealed that in chronic myeloid leukemia (CML) models, the genetic deregulation driving the disease affects a panel of genes regulated by the oncogenes c-MYC and p53, indicating a tumor-related crosstalk between the two pathways, both controlling survival, differentiation, and apoptosis [18]. The gene discussed is TP53; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.