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If someone is considering this approach, working with a licensed provider who can oversee dosing, sourcing, and any side effects is essential

Elevated expression of IGF-IR in BCR/ABL + cells may promote the development and self-renewal of chronic myeloid leukemia, while downregulation of IGF-IR in BCR/ABL + cells leads to acute lymphoblastic leukemia (ALL) [14]

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Taking all this data together it seems logical or appropriate to conclude that, because IGF1-R has a different signalling pathway that can maintain lipid oxidation in the liver, FFA uptake in muscle, and activates mTORC1 could reactivate IR through tyrosine kinase activity on IRS, thus displacing serine phosphorylation, reinstituting insulin signalling