Nonsilent somatic coding mutations exclusive to twin A included a frameshift indel not previously reported in TET2, an epigenetic regulator frequently mutated in hematological cancers, and a stop codon in OTOG associated with nonsyndromic hearing loss18, whereas twin B carried missense mutations in MED27, ENKUR and CEP290 (Fig. 1b and Supplementary Table 4)19. This evidence concerns the gene MED27 and hematopoietic and lymphoid cell neoplasm.