Recently, metformin, an AMPK agonist, was shown to inhibit the metabolism and proliferation of ccRCC cells in several preclinical studies in ccRCC mouse models by Liu M et al. It is also suggested that metformin, under glucose-deficient conditions, promotes the transcription of genes related to cellular metabolism, such as c-Myc, by recruiting pyruvate kinase isozyme type M2 (PKM2) and β-linked proteins to form a complex through AMPK87. This evidence concerns the gene PKM and nonpapillary renal cell carcinoma.