AKT1 and tuberous sclerosis: The potential role of hsa-miR-103a-3p and hsa-miR-494-3p in neurodevelopmental pathologies, such as TSC, has not yet been described, despite hsa-miR-494-3 having been described as a key regulator of endometrial receptivity through the PI3K/AKT/mTOR pathway [77].