ACVR1 and neoplasm: Spatiotemporal genomic mapping of DIPG from whole brain autopsies suggested that the H3K27M histone mutations are often paired with either ACVR1 kinase and/or tumor suppressor TP53 mutations in tumor initiation, followed by later oncogenic alterations often in the phosphoinositide 3-kinases (PI3K) pathway in subclones4.