Overexpression of Mettl3 promotes the growth of ESCC cells, while knockdown may lead to G2/M arrest and inhibit tumor growth through p21 signaling.[85] In addition, it was found that Mettl3 could modify tumor necrosis factor receptor 1 (TNFR1) by m6A, and ataxin-2 could promote TNFR1 protein translation in an m6A-dependent manner. The gene discussed is TNFRSF1A; the disease is neoplasm.