<p>The seed dormancy is an important phenomenon to ensure plant survival under unfavorable conditions, which is regulated by abscisic acid (ABA). In contrast, abscisic acid (ABA) promotes seed dormancy by the activation of signaling cascades that recognized specific receptors. For seed germination its breakup is essential, whereas gibberellic acid (GA) promote germination by opposing ABA effects through intricating the pathways. Henceforth, brassinosteroids (BRs) are recognized an important hormone to be showing enormous role in stimulation of seed germination. However, upon brassinosteroids (BRs) perception by the receptor kinase BRI1 (BRASSINOSTEROID-INSENSITIVE1), it is activated and inactivates the kinase BIN2 (BRASSINOSTEROID-INSENSITIVE 2). If no BR received to BR receptor PYRABACTIN RESISTANCE1/PYR1-LIKE/REGULATORY COMPONENTS OF ABA RECEPTORS (PYR/PYL/RCAR). Reciprocally, in presence of BR the BRASSINOSTEROID INSENSITIVE 1 (BRI1) trigger to inactivating BRASSINOSTEROID INSENSITIVE 2 (BIN2) and initiates dephosphorylation by PROTEIN PHOSPHATASE 2A (PP2A) of BZR1 and BES1 to break the dormancy to activate the regulatory genes bzr1-1D and bes1-D. This signaling cascade underscores the crucial role of BRs in overcoming dormancy, especially under abiotic stress. Meanwhile, ABA-related transcription factors ABI3 and ABI5 promote and sustain dormancy by regulating specific genes such as FUS3, bHLH57, SRK2E/SnRK2.6/OST1, SRK2I/SnRK2.3, PP2C, ABI4 and MYB96 are responsible for promote dormancy and BR pathways genes such as VP1/ABI3, ABI4 and ABI5 are to break the dormancy at DNA level. Additionally, GA is responsible for DELLA proteins accumulate which leading to the suppression of growth-associated genes and the promotion of dormancy-related genes <i>via</i> creating a bridge between GA and BR. These novel insights reveal BRs as pivotal modulators of dormancy release under abiotic stress, offering strategies for enhancing crop establishment, yield, and resilience through BR priming or genetic modulation.</p>