Hormonal IGRs typically work by mimicking or inhibiting the juvenile hormone (JH), one of the two major hormones involved in insect molting. IGRs can also inhibit the other hormone, ecdysone, large peaks of which trigger the insect to molt. If JH is present at the time of molting, the insect molts into a larger larval form; if absent, it molts into a pupa or adult.[1] IGRs that mimic JH can produce premature molting of young immature stages, disrupting larval development.[4] They can also act on eggs, causing sterility, disrupting behavior or disrupting diapause, the process that causes an insect to become dormant before winter.[2] IGRs that inhibit JH production can cause insects to prematurely molt into a nonfunctional adult.[3] IGRs that inhibit ecdysone can cause pupal mortality by interrupting the transformation of larval tissues into adult tissues during the pupal stage.[4]