Given that decreases in muscle fiber protein content may be detected under conditions of maintained muscle fiber size in early clinical cachexia stages [10], and given that, for example, STAT3-dependent SOCS3 upregulation may lead to protein breakdown [27,50], our present finding of a significant increase in the intramyocellular pool of free proteinogenic amino acids with PanIN, but not PDAC, deserves special consideration. The gene discussed is SOCS3; the disease is Cachexia.