The infamous and highly conserved Hippo Network, well known for controlling cell and tissue size, also regulates the size of the tube-shaped tracheal system of the developing fruit fly, but in an unexpected way. Mutations in HN genes cause tracheal size phenotypes that are the opposite of the same mutations in other tissues. For example, a loss-of-function mutation in Yorkie (Yki), the transcription factor regulated by the Hippo Network, yields reduced eye or wing size, due in part to increased apoptosis. However, as we have previously reported, the same Yki mutation causes tracheal overgrowth without affecting cell number. This phenotype is ultimately due to loss of Yki-dependent over-activation of Ice, the fly homologue of the mammalian executioner caspase-3, a protein that is both necessary and sufficient to execute cell death in most cells. Here, we report that activated (cleaved) caspase is enriched at the apical surface of tracheal cells in both wild-type and Yki mutant embryos. This result suggests that the non-apoptotic target(s) of Ice that regulate tube size may also be localized to the apical surface. Moreover, compartmentalization of Ice at the apical surface may allow activation of non-apoptotic targets without cleavage of apoptotic targets. Increased staining of activated Ice is observed in some tracheal tube-size control mutants, and we are presently using this assay to investigate which tracheal genes may regulate tracheal tube size by modulating Ice activity. We also present results from epistasis experiments that explore the complex relationships between and among members of the HN such as Yki and Ice, and known regulators of tracheal size, including components of the septate junction.