It has been recently reported that the biphosphatase TP53-inducible glycolysis and apoptosis regulator (TIGAR) might hold the key for this metabolic reprogramming as overexpression of TIGAR in the breast carcinoma cells boosts the ATP production and glutamine uptake in tumor cells as well as pronounced glycolytic parameters in associated CAFs (238) (Figure 1). This evidence concerns the gene TIGAR and breast carcinoma.