This model addresses three current gaps in CACS modeling: (a) the progressive spontaneous metastatic environment, (b) the full clinical syndrome of progressive wasting of skeletal muscle with altered insulin‐like growth factor‐1 (IGF‐1)/insulin ubiquitin proteasome degradation pathway, adipose tissue wasting, systemic inflammation, anorexia, anemia, hypoalbuminemia, elevated protein breakdown, and metabolic derangement, and (c) sex‐specific temporal cachectic discrepancies. The gene discussed is IGF1; the disease is anemia (phenotype).