The formation of heterochromatin - tightly packed, transcriptionally inactive chromosomal DNA - involves a complex arrangement of histone modifications, including histone H3K9 methylation, which, in flies, is catalysed by the methyltransferase Su(var)3-9. Having observed that hypomorphic mutations in JIL-1 (a histone H3S10 kinase) cause heterochromatin to spread to ectopic chromosomal regions in Drosophila, Johansen and colleagues set out to explain why (see p. 229). To do so, they generated flies that carry both a null and a hypomorphic copy of JIL-1, which almost never survive to adulthood. But when these flies carry an additional copy of the Su(var)3-9 gene that has reduced function, they mostly survive, indicating that Su(var)3-9 and JIL-1 function in the same pathway and are antagonistic. From their results, the authors propose that JIL-1 kinase marks transcriptionally active euchromatin -possibly by phosphorylating histone H3S10 - to prevent Su(var)3-9 from triggering the formation of heterochromatin at ectopic locations.