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922 In AKT-hyperactivated cancer cells, AKT directly phosphorylates the Ser343 site of TRPML1, inhibits the K552 ubiquitination degradation of TRPML1, and promotes the binding of TRPML1 to ARL8B, leading to lysosomal exocytosis

Currently multiple modalities are being approached like silencing certain genes using the RNA interference technology that may have a longer effect than the injectables

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This effect appears to be driven by the glucagon receptor agonism, as glucagon naturally increases heart rate through sympathetic nervous system activation