ZIC1 and medulloblastoma: Our discovery of a H3K27me3/H3K27ac heterozygous chromatin state in G4 medulloblastomas at the ZIC1/ZIC4 locus demonstrates a convincing complementation group in which some tumors achieve repression of ZIC1 through deletion or somatic mutations of genomic DNA, while other tumors reach the same phenotype through chromatin variants that impose epigenetic repression.