In Human many non-­‐Mendelian diseases present a biased sex ratio. It is the case for some neurodevelopmental and psychiatric disorders that male are more prone to develop, as schizophrenia, or autism. On the contrary, women are more susceptible to many autoimmune disorders such as systemic lupus erythematous. With regards to immunity, it has also been observed that males are more prone to infections. Phenotypic robustness (PR), defined as the persistence of a phenotype exposed to genetic or environmental constraints could play a role in disease development. Less robust individuals could express cryptic mutations and also be more receptive to environmental stressors. If there would be a difference of robustness between sexes it could also have an impact on sexually dimorphic disease risk. Some molecular mechanisms could buffer genetic and play a role in phenotypic robustness processes and environmental risk, such as Heat shock proteins (HSP). The aim of this project was to test if a sex difference in phenotypic robustness could be investigated through transcriptional data (RNAseq) from lymphobalstoid cell lines (LCL). Higher expression of HSP or other genes could benefits to a stronger robustness. A more narrow transcriptional regulation in one sex of a gene alongside a smaller variance would indicate a more precise regulation and a possible stronger phenotypical robustness. Gene expression data was generated as RNAseq data LCL from 260 men and 290 women from the CoLaus Study Cohort. 8’924 genes were selected. The statistical analysis was done with R. 268 sex-­‐biased genes with differences of expression were identified, 3.003% of all the tested genes. 31 genes were identified as having a significant difference in variance in expression between sexes, i.e. 0.347% of all the genes tested. Amongst autosomal genes higher variance in expression was observed for males in 8 genes and in females in 10 genes. No significant trend of a conserved sex-­‐biased variance was identified. In X genes 13 genes showed a higher variance in women and none in men. Isoform distribution between males and females was compared for the 31 genes in in order to determine if it was part of the etiology of the variance differences. Significant differences in isoform distribution were found in 1 autosomal gene. 4 HSP genes showed a sex-­‐biased expression, 3 female-­‐biased and one male-­‐biased. 320 Immune-­‐related genes were also specifically screened for differences in expression and in variance in expression. 23 autosomal genes were identified as sex-­‐biased and none with a difference in variance in expression. Some HSP levels could differ between sexes and play a role in phenotypic robustness process. This study showed small but significant sex-­‐biased expression of HSP in LCL and further analyses of other tissues should be conducted as some HSP might also be regulated by hormonal signals. At the regulation level this RNAseq all-­‐transcriptome screening for sex-­‐specific patterns of regulation did not show a sex-­‐biased trend. Isoforms analysis between sex did not show significant differences in pattern distribution. This mean that the hypothesis of a general sex-­‐ specific pattern of regulation leading to a differential robustness mechanisms is unlikely, although the sex-­‐biased expression of specific genes could still play a role. An alternative option would be that LCL could also not be appropriate to measure it.