In this context, it is plausible to view PEP as a rheostat of either glucose carbon flux or cataplerotic fluxes (i.e., PEPCK-M) from other carbons sources such as glutamine, to “inform” on the availability of biosynthetic precursors of the glycolytic pool, such as serine and glycine, to cope with sustenance and growth at various stages of tumor development. Here, PCK2 is linked to neoplasm.