To investigate whether the differential oncogenic effects observed between PRPS2 and PRPS1 result from their enzymatic catalysis affecting the abundance of metabolic flux through the purine biosynthesis pathway, we conducted liquid chromatography tandem mass spectrometry (LC-MS/MS)-based metabolite isotopic tracer profiling along the purine biosynthesis pathway in H1299 lung cancer cells ectopically expressing PRPS2 or PRPS1 (Fig. 3a). This evidence concerns the gene PRPS1 and lung cancer.