These metabolic features cause protein catabolic demolition of both skeletal muscular and globular (i.e., albumin, hemoglobin, immunoglobulins, etc.)proteins, such as AAs, and are consumed mostly to support the increased global energetic needs, rather than being available for protein synthesis and function, with consequent proteinic metabolism disarrangements, which are clinically evident in sarcopenia and worsen the patient prognosis [20]. The gene discussed is ALB; the disease is sarcopenia.