KMT2A and neoplasm: Fluorescence in situ hybridization (FISH) analyses demonstrated that the tumor cells were negative for amplification of MDM2 (Fig. 3E), and rearrangements of FUS (Fig. 3F), EWSR1, and KMT2A. Genetic testing using targeted next-generation sequencing (NGS) for 425 cancer-relevant genes (Gene seqPrime) revealed a low tumor mutation burden (TMB) (1.1 mutations per megabase) and a likely pathogenic mutation of CYP2B6 (NM_000767.5) at chromosome 19:41,515,212 of exon5 c.734T > C(p.I245T, missense variant), which has a variant allele frequency (VAF) of 25.0 % (Fig. 4).