Knockdown of HCA3 induces a significant cell death and cell viability reduction in three breast cancer cells: BT-474, HCC1954 and HCC38.136 Here is one possible explanation: cancer cells shunt glucose to anabolic processes instead of oxidizing glucose to produce ATP, then energy needs must be met in other ways, such as FAO.2 By increasing lipolysis and subsequent FAO, acetyl-CoA which can enter the citric acid cycle is produced.2 When the level of acetyl-CoA exceeds the need of the citric acid cycle, ketone bodies (such as 3HB) are generated. This evidence concerns the gene HCAR3 and breast carcinoma.