Not only mTORC1, but also mTORC2 activity has been linked to health and lifespan. Rictor, an important component of mTORC2, contributes to glucose homeostasis in murine muscle tissue (Bentzinger et al., 2008). TORC2 C. elegans mutants show modulation of feeding and metabolism of different diets by affecting (Soukas et al., 2009). TORC2 is a mediator of proliferative and survival signals in cancer cells (Fang et al., 2012), and a study in mouse fibroblasts showed that mTORC2 regulates the TLR-mediated inflammatory response via FoxO1 (Brown et al., 2011). In additionof random permutations to calculate an empirical P-value for the observed SNP set statistic. In our analysis, we used a setmax of 5, a set-P of 0.01 and a set-r2 of 0.5. The SNP sets were defined as the 10-kb regions upstream and downstream of the genes in the mTOR pathway (Fig. 1). The analysis was performed separately for nonagenarians vs. controls and offspring vs. controls, including age (in offspring vs. controls only) and gender and their interaction as covariates.The text seems to be a scientific article discussing the association between gene expression and insulin-related phenotypes. Here is the processed text:

The study analysed simulated SNP sets in which the phenotype status of individuals was permuted. An empirical P-value for the SNP set was computed by calculating the number of times the test statistic of the simulated SNP sets exceeded that of the original SNP set. The parameters used were setP = 0.05, set-r2 = 0.5, set-max = 99 999, and mperm = 10 000. Bonferroni correction for the pathway analysis was not necessary as it contained just one test. When SNP sets were tested per gene (40 SNP sets), the significance level for P-values after Bonferroni correction for multiple testing was 0.00125.

Since the mTOR pathway has been implicated in insulin-related phenotypes, its effect on the expression of longevity-related genes was investigated. Blood samples were taken at baseline to determine non-fasted serum parameters using Hitachi Modular or Cobas Integra 800, both from Roche, Almere, the Netherlands. CVs of these measurements were all below 5%. Information on medical history was requested from participants' general practitioners. Differences in expression level between offspring and controls were assessed using linear regression with the same model but excluding known Type 2 diabetes patients. The association of glucose and insulin levels with expression levels of seven longevity-associated genes was also analysed using linear regression in controls only. To investigate the influence of glucose and insulin levels on the association with longevity of these seven genes, linear regression between offspring and controls was performed again, including one of these parameters as a covariate.