“…As suggested before [124], technical advances relying, for example, on new tools using the Cre/loxP recombination system in mice will permit better investigation of the intricacies of SHIP1 regulation in vivo-whereby such a genetic approach has already been applied for several innate immune populations [55,65,85,110], and is increasingly available for rarer immune subsets [125][126][127][128]. In particular, the role of SHIP1 in limiting type 2 responses is clear, as evidenced by its effect in macrophages, basophils, MCs, ILC2s, and eosinophils [123,124,129], possibly further increasing the relevance of SHIP1 to type 2-driven inflammation for diseases at barrier sites. SHIP1 is generally seen as a negative regulator for PI3K signaling due to its ability to reduce intracellular PI (3,4,5) P 3 levels.…”