In parallel, PGC1α KO iMEFs helped to form larger and more proliferative primary tumors than WT counterparts and fostered the formation of lung metastasis by B16 melanoma cells (112), which indicated that the metabolic adaption in response to the knockdown of PGC1α and mitochondrial functional deficiency in CAFs played a tumor-facilitative role in melanoma progression. The gene discussed is PPARGC1A; the disease is neoplasm.