Insect bodies are subdivided into anterior (A) and posterior (P) compartments: cohesive fields of distinct cell lineage and cell affinity . Like organs in many animal species, compartments can develop to normal sizes despite considerable variation in cell division . This implies that overall compartment dimensions are subject to genetic control, but the mechanisms are unknown. Here, studying Drosophila's embryonic segments, I show that P compartment dimensions depend on epidermal growth factor receptor (EGFR) signaling. I suggest the primary activating ligand is Spitz, emanating from neighboring A compartment cells. Spi/EGFR activity stimulates P compartment cell enlargement and survival, but evidence is presented that Spitz is secreted in limited amounts, so that increasing the number of cells within the P compartment causes the per-cell Spitz level to drop. This leads to compensatory apoptosis and cell-size reductions that preserve compartment dimensions. Conversely, I propose that lowering P compartment cell numbers enhances per-cell Spitz availability; this increases cell survival and cell size, again safeguarding compartment size. The results argue that the gauging of P compartment size is due, at least in part, to cells surviving and growing according to Spi availability. These data offer mechanistic insight into how diffusible molecules control organ size.