Understanding how genetic differences affect phenotypic variation within and between species is a central goal of evolutionary and medical genetics. Gene regulatory differences are thought to be the primary contributors to phenotypic differences between human and chimpanzee. Yet, to date, essentially all such studies of gene regulatory differences between species have focused on mRNA expression and transcriptional regulation rather than protein abundance. Yet, proteins are subject to post-transcriptional and post-translational regulation, not revealed by mRNA measurements alone. Ultimately, proteins perform much of the work of the cell and likely more direct targets of selection. In the first part of the talk, I describe a novel method for measuring the differential levels of two alleles, or protein allele-specific expression (ASE), in a viable hybrid between distantly related yeast species using high-resolution, quantitative mass spectrometry. The method allows the first analysis of the contribution of cis-regulatory and trans-regulatory differences to protein abundance divergence between species. In the second part of the talk, I describe a study of mRNA expression and protein abundance divergence between human, chimpanzee, and rhesus macaque using RNA-seq and high-resolution, quantitative mass spectrometry data collected from lymphoblastoid cell lines. Our results show that protein abundance levels between primates evolve under much stronger evolutionary constraint than mRNA expression levels. We use data from all three species to computationally identify genes whose regulation might have evolved under natural selection, and considered jointly, our data allowed us to identify genes where lineage-specific changes might specifically affect post-transcriptional or post-translational regulation. Taken together, our results indicate that on an evolutionary timescale, there is surprising flexibility in primate mRNA levels, as these changes are very often either buffered or compensated for at the protein level.