This article compares several post-1950s translations of the Liezi, and examines the concept of originality, the degrees of closeness to the original text a modern translation can achieve, and how this “faithfulness” can be understood. I first discuss how the problem of the Liezi's originality has negatively influenced critics' and translators' perception of the text's significance, then compare its different translations to show their specific translational and interpretational problems. Finally, I reflect on the overarching methodological question that frames my comparisons of translations, namely, why compare? I argue that comparing translations cannot be a means to ascertain the best translation, because both concepts of originality and faithfulness are multiple in meaning rather than singularly defined. Instead of measuring translations in terms of “fidelity,” a more insightful practice would be discovering the insights different translations offer into the relationships between the original and translated texts, source and target languages, as well as questioning the construction of texts as “original source texts” through translation by recognizing the potential fluidity and multiplicity of the source text itself.

The translational apparatus very efficiently eliminates errors that would cause a spontaneous shift in frames. The probability of frameshifting can be increased dramatically by either cis or trans-acting factors. Programmed translational frameshift sites are cis-acting sequences that greatly increase the frequency of such errors, at least in part by causing a transient translational pause. Pausing during programmed +1 frameshifts occurs because of slow recognition of the codon following the last read in the normal frame. Frameshifting can also be elevated in strains carrying mutations in the homologous elongation factors EF-Tu in bacteria, and EF-1α in the yeast Saccharomyces cerevisiae. This phenotype implies that the factors contribute to frame maintenance. Because EF-Tu/EF-1α modulate the kinetics of decoding, it is possible that the frameshift suppressor forms of the factors transiently slow normal decoding, allowing spontaneous frameshifting to occur more efficiently, resulting in phenotypic suppression. We have used a set of frameshift reporter plasmids to test the effect of suppressor forms of EF-1α on constructs that differ widely in the efficiency with which they stimulate +1 shifting. When these results were compared to the effect of increased translational pausing, it was apparent that the mutations affecting EF-1α do not simply prolong the translational pause. Rather, they appear to generally increase the likelihood of frame errors, apparently by affecting the error correction mechanism of the ribosome.