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. Here, INS is linked to anemia (phenotype).