Additionally, despite the initial efficacy of FGFR3‐targeted agents like erdafitinib, their clinical benefit is often limited by the emergence of secondary mutations and bypass signaling mechanisms, leading to drug resistance.[11] These characteristics establish both FGFR3 and MAD2L1 as compelling therapeutic targets in BC. Consequently, there is an urgent need to develop therapeutic approaches capable of overcoming these molecularly driven challenges. The gene discussed is MAD2L1; the disease is breast cancer.