In 2010, Margaret E Benny Klimek et al. first identified the potential of ACVR2B-Fc, an artificial fusion protein that has the extracellular domain of the ACVR2B fused to human Fc, acting as an antagonist of the ACVR2B signaling, in attenuating cachemia in both colon-26 and Lewis lung carcinoma, with no influence on the progression of tumors [29]. The gene discussed is ACVR2B; the disease is Carcinoma, Lewis Lung.