PLAGL1 and neoplasm: For example, the tumor-driving H3.3K27M mutation in pediatric diffuse intrinsic pontine gliomas (DIPGs) results in the inactivation of the PRC2 complex, causing ectopic expression of LIN28B, PLAG1, and PLAGL1, and leading to the de-differentiation and hyperproliferation of tumor cells [32–34].