Evolution of insect resistance is the primary threat to the long‐term efficacy of
Bacillus thuringiensis
(Bt) transgene technologies. Plants have a deeply conserved defence response to pests: Jasmonic acid (JA) hormone signalling mediated by transcriptional repressors called JASMONATE‐ZIM‐DOMAIN/JAZ. JAZs normally limit expression of plant defence pathways, promoting assimilate partitioning towards growth and reproduction, by their carboxyl terminal Jas motif that antagonises MYeloCytomatosis (MYC) master transcription factor activities. Deletion, alternative splicing/intron retention, or disruption of the Jas motif results in JA insensitivity and increased resistance to pathogens including arthropod herbivores, for example by production of secondary metabolites and new leaves with higher trichome density. JA‐mediated trichome initiation and elongation also impact cotton fibre production. Since its release in 2017, the third‐generation stacked commercial Bt insecticidal Vip3A protein traits are increasingly under severe pressure for evolution of
Helicoverpa zea
(bollworm) resistance. Regional differences in efficacy of Bollgard
®
3 and WideStrike
®
3 against lepidopteran pests and increasing pesticide use are emerging issues. Future transgenic field control failures from bollworm infestations and incursions of
Helicoverpa armigera
from Central America are likely in the U.S. Cotton Belt. In this systematic primer on the problem, we take a conceptual approach to consider
JAZ
genes as means to leverage ‘internal’ host‐derived herbivore resistance in cotton. We consider the genetic redundancy and pleiotropic nature of JAZ master regulators on tissue‐specific growth, development, crosstalk with hormonal and small RNA pathways as nodes in networks, and limitations of JAZ efficacy due to fitness costs/growth trade‐offs versus prospects for enhancing resistance networks to orchestrate transgressive segregation (generation of extreme phenotypes in breeding progeny not seen in parental lines).