Congratulations to Jamie Wilson (a Wellcome Trust Clinical Fellow in John Rouse's lab) who made a big advance in understanding SLX4 with help from Agueda Tejera in Maria Blasco's lab at CNIO, Madrid. He showed that around half of the SLX4 complex localizes constitutively at chromosome ends. This is mediated by a new motif we identified in SLX4 that interacts with the telomere binding protein TRF2. Mutations in this motif release SLX4 complex from telomeres. Jamie also found that the proper localization of SLX4 at telomeres is required to prevent telomeres from becoming too long. Mutations that release SLX4 from telomeres cause telomeres lengthening, and they cause telomere fragility and damage. These data indicate that the SLX4 complex acts as a sensor of telomere length and mediates "telomere trimming". Jamie's data were published recently in Cell Reports