Moreover, METTL16 KO-mediated growth inhibition could be also partially reverted by forced expression of catalytically inactive (PP185/186AA [25, 44]) METTL16 (sgRNA-resistant) (Additional file 1: Fig. S2L–N), suggesting both the methyltransferase-dependent and -independent functions of METTL16 contribute to its robust tumor-promoting role in HCC. Here, METTL16 is linked to neoplasm.