The inference that the observed mutational variance was typically due to small effect mutations was further supported by the observation that the largest mutational effect sizes were <1 phenotypic standard deviation for most expression traits (3112, corresponding to 91.9% of variable traits).
The pathogenicity of the mutations was further corroborated by the high conservation of the mutated amino acids.
The significance (P value) of co-occurring or anti-co-occurring cancer gene mutations was further determined using Fisher's exact test based on the obtained four numbers.
The stability of the introduced mutations was further checked in viruses recovered from latently infected spleens confirming the retention of the engineered point mutations.
The mechanistic importance of truncating exon 9 mutations was further expanded by Fratter et al. (2011), who showed that three further novel pathogenic variants in exon 9 caused familial autosomal-dominant PEO in seven unrelated probands.
The notion that subgroups of ependymoma arise from regionally and developmentally distinct RGCs that have undergone transformation by subgroup-specific genetic mutations was further confirmed functionally in the case of supratentorial ependymomas.
