Additionally, while IGF-1 was able to counteract Ang II-regulated MAFbx expression via Akt-dependent FoxO1 repression, IGF-1 was unable to abolish MuRF1 up regulation [49], thus suggesting prevalence of TFEB in controlling MuRF1 expression in Ang II-dependent skeletal muscle atrophy. The gene discussed is IGF1; the disease is muscular atrophy.