In contrast, our data indicate that the other two type I PRMT proteins, PRMT4 and PRMT6, are counter-targets for persistent cancer cells: their knockdowns and/or pharmacological inhibitions promoted persistence across multiple EGFRmut and KRASG12C lung cancer cell lines (Figs. 1A and 2A; Supplementary Figs. S1B, S2B, and S2C). This evidence concerns the gene CARM1 and lung carcinoma.