Next, epigenetic analysis via LC-MS/MS reveals higher m6A-abundance in ALKBH5-deficient as compared to FTO-deficient B16 tumours, which meaningfully suppresses the expression of m6A-mediated ‘Mct4/Slc16a3’ in ALKBH5 alone and ‘Mex3d’ in ALKBH5 and FTO both. Here, SLC16A3 is linked to neoplasm.