However, studies have shown that functional redundancy exists between MCT1 and MCT4, and genetic silencing or pharmacological inhibition of MCT1 in human colon adenocarcinoma cells was effective only when combined with MCT4 depletion (Le Floch et al., 2011; Marchiq and Pouysségur, 2015). This evidence concerns the gene SLC16A1 and colon adenocarcinoma.