LRRC4 and neoplasm: By employing GCs from LRRC4 knockout mice and KGN cells (a human granulosa‐like tumor cell line), as well as a cyclophosphamide (CTX)‐induced POI model, our study reveals the novel pathogenesis of POI that LRRC4 balances mitochondrial fission and fusion to maintain mitochondrial metabolic homeostasis by promoting the ubiquitination degradation of YAP.