Probably, compensation mechanisms of MCT1-mediated lactate transport by MCT4 function [37], as well as the occurrence of a reverse Warburg effect phenotype upon reprogrammed metabolic requirements–in which MCT1 mediates lactate import to fuel OXPHOS in cancer cells [13]–explain unique metabolic dependencies in these malignancies that are ultimately translated to the clinical setting. This evidence concerns the gene SLC16A1 and cancer.