Furthermore, H3.3K27M can substitute for H3.1K27M mutation and cooperate with ACVR1 R206H in tumor initiation as mice that were infected with ACVR1 R206H, H3.3K27M, Cre, and PDGFA also had a high tumor incidence (20/22 = 91%) similar to ACVR1 R206H, H3.1K27M, Cre, and PDGFA. This evidence concerns the gene ACVR1 and neoplasm.