Nevertheless, H3 K27me3 loss resulting from pharmacological EZH2 inhibition and intrinsic mechanisms can lead to opposite outcomes, as it was shown in H3 K27M-mutant diffuse midline glioma cell lines.36 However, other studies showed that EZH2 can also act as a tumor suppressor in this tumor, depending on the genetic context, and EPZ-6438 can even promote tumor cell proliferation.37 In conclusion, our results should be extrapolated with caution to meningiomas that, unlike the IOMM-Lee cells, show H3 K27me3 loss. The gene discussed is EZH2; the disease is meningioma.