Collectively, these results suggest that ALKBH5 and FTO target metabolic genes and increase the expression of Mct4/Slc16a3 and Mex3d (supplementing lactate to the tumour) by inhibiting m6A methylation-mediated RNA-splicing mechanisms, supported by Zaho et al., 2014 [167], (Figure 6, therapeutic model). The gene discussed is SLC16A3; the disease is neoplasm.