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. 2018 Aug 13;3:22. doi: 10.1038/s41525-018-0061-8

Table 2.

Mutations and affected genes identified for each subject

Subject Gene Variant ACMG variant classificationa Genomic location Novel gene/known EIEE gene/previously reported
1 KCNQ2 c.841G>A, p.G281R Pathogenic (PS1, PS2, PM2, PP3, PP5) chr20:62071037 Known gene, previously reported mutation43,55
2 Multiple Balanced inverted translocation between Chr2 and ChrX chrX:151118513
chr2:59405748
Novel structural mutation similar to previously structural rearrangement42
3 SCN8A c.1219T>G, p.L407V Pathogenic (PS2, PM2, PM5, PP2, PP3) chr12:52099285 Known gene, previously reported mutation at this site56
4 PIGA c.502A>C, p.N168H Likely pathogenic (PS2, PM2, PP3) chrX:15349551 Known gene, novel mutation
5 SCN8A c.800T>C, p.L267S Likely pathogenic (PS2, PM2, PP2, PP3, PP5) chr12:52093447 Known gene, novel mutation (same patient and mutation reported concurrently in Malcolmson et al.57)
6 EEF1A2 c.1267C>T, p.R423C Pathogenic (PS1, PS2, PM2, PP3) chr20:62119776 Known gene, previously reported mutation58
7 CDKL5 c.146-14735_2276+3273dup Pathogenic (PVS1, PS2, PM2, PP3, PP5) chrX:18567862 -18630963 Known gene with previously reported loss of function mutations2830
8 SCN2A c.647T>G, p.L216W Likely pathogenic (PS2, PM2, PP2, PP3) chr2:166165903 Known gene, novel mutation
9 DEAF1 c.634G>A, p.G212S Pathogenic (PS1, PS2, PS3, PM2, PP3, PP2) chr11:687941 Known gene, previously reported mutation33
10 CAMK2G c.719C>T, p.T240M Likely pathogenic (PS2, PM2, PP2, PP3) chr10:75607083 Novel gene
11 STXBP1 c.1151dup, p.D385Gfs*19 Pathogenic (PVS1, PS2, PM2, PP3) chr9:130438123 Known gene, previously reported loss of function mutations33,43
12 SCN8A c.2642T>C, p.V881A Likely pathogenic (PS2, PM2, PP2, PP3, PP5) chr12:52159552 Known gene, novel mutation
13 SCN1A c.4736T>C, p.L1590P Likely pathogenic (PS2, PM2, PP2, PP3) chr2:166850739 Known gene, novel mutation
14 KCNQ2 c.833T>C, p.I278T Likely pathogenic (PS2, PM1, PM2, PP3) chr20:62071045 Known gene, novel mutation

aPVS1—Null variant (nonsense, frameshift, canonical ±1 or 2 splice sites, initiation codon, single or multi-exon deletion) in a gene where LOF is a known mechanism of disease

PS1—Same amino acid change as a previously established pathogenic variant regardless of nucleotide change

PS2—De novo (both maternity and paternity confirmed) in a patient with the disease and no family history

PS3—Well-established in vitro or in vivo functional studies supportive of a damaging effect on the gene or gene product

PS4—Prevalence of the variant in affected individuals is significantly increased compared with the prevalence in controls

PM1—Located in a mutational hot spot and/or critical and well-established functional domain (e.g., active site of an enzyme) without benign variation

PM2—Absent from controls (or at extremely low frequency if recessive) in Exome Sequencing Project, 1000 Genomes Project, or Exome Aggregation Consortium

PM5—Novel missense change at an amino acid residue where a different missense change determined to be pathogenic has been seen before

PP2—Missense variant in a gene that has a low rate of benign missense variation and in which missense variants are a common mechanism of disease

PP3—Multiple lines of computational evidence support a deleterious effect on the gene or gene product (conservation, evolutionary, splicing impact, etc.)

PP5—Reputable source recently reports variant as pathogenic, but the evidence is not available to the laboratory to perform an independent evaluation