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Intriguingly, the transcriptional profiling of tumors showed that PCPGs can be divided into two clusters: a “pseudohypoxic” cluster that includes tumors with von Hippel–Lindau tumor suppressor (VHL) and succinate dehydrogenase (SDHx) mutations and an “activated tyrosine kinase” cluster, mainly associated with aberrations in ret proto-oncogene(RET) and neurofibromatosis type-1 (NF1) [114]