Previously, Segev and Gerst found that mutants in any of the four ribosomal protein genes rpl1b, rpl2b, rps11a, or rps26b had a petite phenotype-i.e., the mutants were deficient in respiration. Strikingly, mutants of their paralogs rpl1a, rpl2a, rps11b, and rps26a were grande-i.e., competent for respiration. It is remarkable that these paralogs should have opposite phenotypes, because three of the paralog pairs (Rpl1a/Rpl1b, Rpl2a/Rpl2b, Rps11a/Rps11b) are 100% identical to each other in terms of their amino acid sequences, while Rps26a and Rps26b differ in 2 amino acids out of 119. However, while attempting to use this paralog-specific petite phenotype in an unrelated experiment, I found that the rpl1b, rpl2b, rps11a, and rps26b deletion mutants are competent for respiration, contrary to the findings of Segev and Gerst.