A report by Suriben and colleagues, in 2020, demonstrated that inhibition of GDF15 activation of GFRAL in the brainstem, using a monoclonal antibody (3P10) that inhibited RET recruitment to the GDF15–GFRAL complex, significantly curtailed excessive lipid oxidation in several murine cancer cachexia models [76]. The gene discussed is GFRAL; the disease is Cachexia.