In human adenomyosis tissues, LC3B reduction was confined to the stromal compartment of ectopic lesions, whereas glandular and eutopic endometrium remained comparable to controls, indicating a persistent stromal-specific alteration of autophagy-associated markers.<h4>Conclusions</h4>Modulation of autophagy-associated markers is an early and transient event in murine adenomyosis initiation, whereas in human disease, stromal-specific LC3B reduction persists in established lesions. Here, MAP1LC3B is linked to adenomyosis.