Molecularly, GBs are characterized by isocitrate dehydrogenase wild-type (IDH-wt) status, telomerase reverse transcriptase (TERT) promoter mutations, epidermal growth factor receptor (EGFR) amplification and chromosomal alterations,4‐6 while HGA are identified by mutations in isocitrate dehydrogenase 1 and 2 (IDH1-2), alpha thalassemia/mental retardation syndrome X-linked (ATRX), tumor protein p53 (TP53) and cyclin-dependent kinase inhibitors 2A and 2B (CDK2A/B).7 This evidence concerns the gene IDH1 and human granulocytic anaplasmosis.