Pancreatic cancer (PC) has the highest mortality rate of all cancers with the 5-year survival rate at only 13%. In about 15% of newly diagnosed cases where the tumor is non-metastatic and resectable, most patients will ultimately develop tumor recurrence that is usually associated with rapid development of cachexia, a wasting syndrome that features a complex metabolic disorder with progressive weight loss, muscle atrophy, fatigue, weakness, and significant loss of appetite. Recent studies indicate that ameliorating muscle wasting could significantly improve cancer survival. Recently, we established a mouse model for curative surgical resection of PC, in which distal pancreatectomy was performed to remove orthotopic PC xenografts. We demonstrated that surgical resection at early stage of PC improved mouse survival and overall health, which closely mimics human disease. If combined with other therapies such as molecularly targeted therapy and chemotherapy, we hypothesize that the outcome could be further improved, especially if muscle wasting is ameliorated. We recently identified a zinc transporter, ZIP4, as a novel therapeutic target in PC. The essential micronutrient zinc is a required co-factor for many transcription factors and plays a critical role in cancer. Dysregulated zinc transport has been implicated in several cancers. We demonstrated that ZIP4 is over-expressed in the majority of human PC and contributes to tumor growth and metastasis. ZIP4 expression also correlates with tumor progression and survival in PC mouse models, and in human PC, suggesting that ZIP4 is a potential target for PC treatment.