Given the result that the survival of mice in the C26 model was correlated with the suppression of Il6ra in Gfral+ neurons in the AP (Fig. 6d), and previous findings that Gfral and its ligand GDF-15 (Growth/differentiation factor 15) are involved in cancer cachexia10,11, we reasoned that the activity of Gfral+ AP neurons contributes to the development of this syndrome. The gene discussed is MICE; the disease is cancer.