Promoter-proximal pausing, a block to elongation in which RNA polymerase II(Pol II) pauses downstream of the promoter, regulates the transcription of many eukaryotic genes. One recent model suggests that, in Drosophila,JIL-1-dependent phosphorylation of histone H3 at serine 10 (H3S10) releases Pol II from promoter-proximal pausing. But, on p. 2917, Kristen Johansen and colleagues comprehensively refute this model and suggest instead that the transcriptional defects seen in JIL-1 null fly mutants are caused by global chromatin structure alterations. Using several histone H3S10 phosphorylation antibodies and an acid-free polytene chromosome squash protocol, the researchers show that there is no redistribution or upregulation of JIL-1 or histone H3S10 phosphorylation in transcriptionally active puffs in heat-shocked Drosophila salivary glands. They also show that the elongating form of Pol II is present at heat-shock induced puffs in JIL-1 null mutants and that Hsp70 mRNA is robustly transcribed in these mutants. Thus, they conclude, JIL-1-mediated histone H3S10 phosphorylation is not required for Pol II-mediated transcription at active loci in Drosophila.