inx2^G0016 mutant embryos are much smaller than wild type. Many epithelial tissues that invaginate during development, including the hindgut, the Malpighian tubules, the salivary glands, and the tracheal system are reduced in size, and the foregut epithelium is almost completely lost. Germline clone inx2^G0016 mutant embryos, which lack both maternal and zygotic inx2 function, fail to form cuticle and have severely affected epithelial tissues and organs. These mutants also exhibit extensive cell death. inx2^G0016/+ embryos, whose wild-type copy of inx2 is paternal, show few epithelial defects and reduced cell lethality compared to homozygotes. These maternal null, zygotic heterozygous inx2^G0016 mutants display large holes in the head region and show a variable spectrum of segment defects. Cells affected in the head region of zygotic inx2^G0016 mutants appear round, as they seem to have lost polarity.

Mutant larvae show a feeding defect. About two-thirds of mutant animals die as embryos and one-third die during the first larval instar. The ectodermal cells that would normally form the "keyhole" structure during proventriculus development stay fixed within the tightly organised epithelial foregut tube in mutant embryos until late stages of development and the migration of these cells into the endodermal pouch (which occurs in wild-type embryos) does not occur.

Lethality occurs during the embryonic stage and the first larval instar.