HOX genes are transcription factors that specify identity along the animal anterior-posterior axis. Their disruption can cause striking homeotic transformations – for instance, loss of Ubx transforms the third thoracic segment of Drosophila into another second segment, converting halteres to wings. How Ubx promotes haltere and suppresses wing development remains incompletely understood, and is the subject of Barry Thompson and colleagues’ new paper. The authors had previously shown that proteolytic remodelling of the extracellular matrix (ECM) drives wing morphogenesis and is repressed by Ubx in the haltere. They now show that two apical ECM (aECM) proteases, Stubble (Sb) and Notopleural (Np), are expressed in the wing and repressed in the haltere by Ubx. The aECM is remodelled twice in pupal development to allow wing expansion and elongation (in which Np plays a key role). In halteres, Ubx directly binds the regulatory regions of Sb and Np, and also two basal ECM (bECM) proteases Mmp1 and Mmp2 and their inhibitor Timp. Timp expression in the haltere is dependent on Ubx, and knockdown of Sb and Np combined with overexpression of Timp leads to a haltere-like phenotype in the wing (mimicking the effect of Ubx overexpression). Thus, Ubx controls morphogenesis via the matrix both negatively (in repressing aECM proteases) and positively (in promoting a bECM protease inhibitor).