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HGF/c-Met signaling is a well-established oncogenic pathway: c-Met is amplified or overexpressed in multiple cancers (gastric, lung, renal, hepatocellular) HGF/c-Met activation promotes tumor cell proliferation, survival, invasion, and metastasis c-Met inhibitors are FDA-approved cancer drugs (cabozantinib, crizotinib, capmatinib) A compound that potentiates HGF/c-Met signaling raises theoretical concerns about promoting tumor growth or transformation with chronic use

Improved vascular endothelial function after oral B vitamins: An effect mediated through reduced concentrations of free plasma homocysteine

Nuclear lamins: Thin filaments with major functions

Glutamate dehydrogenase 1 (GLUD1)

Often depleted by birth control pills

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