We also found that ROS1 knockdown led to marked downregulation of LDHA (Figure 7G), suggesting that ROS1 can modulate the expression of LDHA. This is consistent with the idea that cancer cells maximize ATP production by both glycolysis and OXPHOS, resulting in the utilization of different nutrients and an increase in metabolic plasticity to maintain tumor survival and metastasis during different stages of disease progression [20]. This evidence concerns the gene ROS1 and neoplasm.