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Activation of this pathway results in protein synthesis, hypertrophy and inhibition of the key ubiquitin ligase atrogin-1 by inactivating Foxo factors[82], IGF-IR also phosphorylates Shc, which subsequently activates the RAS/Raf/MEK pathway leading to cell proliferation and mitogenesis[2]
Combining them raises the theoretical risk of additive or even synergistic hepatocellular stress through at least two overlapping mechanisms