One essential hallmark of tumour cells is altered metabolism (1). Most tumour cells exhibit high rates of glycolysis, even in the presence of oxygen (“Warburg effect”), resulting in increased production of lactate, which is transported out of the cells, contributing to the acidic microenvironment encountered in tumours. The acidic microenvironment has been associated with invasive behaviour, mutagenesis as well as radio- and chemoresistance (2). More recently, several authors have proposed a metabolic complementarity between tumour and stroma. If the tumour is glycolytic, the associated stroma is more oxidative and vice-versa. The latter process is known as the “reverse Warburg effect” (3). Monocarboxylate transporters (MCTs), by performing the plasma membrane efflux of lactate coupled with a proton, especially the isoforms 1 (MCT1) and 4 (MCT4), play an important role in the maintenance of the metabolic phenotype of tumours and associated stroma. MCT1 has been more associated with cells exhibiting an oxidative phenotype, being involved in lactate uptake, while MCT4 has been associated with the glycolytic phenotype, being responsible for lactate efflux (4). Our group has been studying the expression of these MCT isoforms as well as their chaperone, CD147, essential for MCT activity and plasma membrane expression, in several series of human cancers (5). We found upregulation of MCT1 and MCT4 colorectal cancer, upregulation of MCT1, MCT4 and CD147 in cervical cancer, upregulation of MCT1 in breast cancer and upregulation of MCT1 and CD147 in glioblastomas, compared to the corresponding non-neoplastic tissues. On the other hand, there was downregulation of MCT4 in gastric cancer and downregulation of MCT1 in prostate cancer. We also found important associations between MCT overexpression and the clinicopathological data of the cases, mostly with aggressiveness parameters. Due to their role in the maintenance of tumour metabolism, MCTs are considered promising targets in cancer therapy. Thus, we are also studying the effects of MCT inhibition using different tumour models. In general, MCT inhibition in glycolytic tumour cells leads to a decrease in lactate production, cell proliferation, migration and invasiveness (6). In summary, MCT activity is essential for the maintenance of the metabolic phenotype of tumours, playing a key role in the crosstalk between tumour cells and microenvironment. However, MCTs are differentially expressed among the solid tumours and future strategies of MCT inhibition in cancer treatment should take this fact into account.