In the previous section, the established participation of paraspeckles in cancer was demonstrated using the CML context, where BCR–ABL, the main cause of a vast majority of CMLs [21], tends to activate c-Myc, which then represses NEAT1, which in turn prevents paraspeckle formation. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.