Then, we treated U87 or U251 cells overexpressing or knocking down METTL14 with actinomycin D, and found that compared with control cells, the half-lives of the ASS1 precursor and mature mRNA in glioma cells were significantly reduced by transfection with the METTL14 overexpression plasmid, while inhibition of METTL14 showed the opposite result (Figure 5f, g). The gene discussed is METTL14; the disease is glioma.