In CIC-DUX4 sarcomas, the negative feedback loop of ERK/CIC/DUSP6 turns into a positive feedback axis, where the CIC-DUX4 fusion product leads to overexpression of DUSP6 and shut down of ERK signaling, promoting CIC-DUX4 retention in the nucleus and its target genes transcription [55]. The gene discussed is DUSP6; the disease is sarcoma.