This protective mechanism is due to increased activation of the IGF-1/Akt/mammalian Ray mTOR pathway, which blocks AT1 (vascular tension) (Prime type) receptors can improve muscle remodeling and prevent disuse atrophy and may prove to have clinical benefits against injury-related muscle remodeling and provide prevention of disuse atrophy for people with secondary sarcopenia protection. The gene discussed is IGF1; the disease is sarcopenia.