In addition, recent studies have found that CAFs can create a nutrient-rich microenvironment via the local stromal generation of mitochondrial fuels, such as lactate, glutamine, and fatty acids, to metabolically support cancer development, and HIF1-α serves as a tumor promoter in CAFs in this metabolic coupling between CAFs and cancer cells [23, 24]. This evidence concerns the gene HIF1A and neoplasm.