ACTL7A (actin-like 7A) is essential for male fertility and normal spermatogenesis 1. The protein functions primarily in acrosome biogenesis and sperm head morphology, where it anchors and stabilizes acrosomal adherence to the acroplaxome by facilitating F-actin in the subacrosomal space 2. ACTL7A also plays a critical role in formation and fusion of Golgi-derived vesicles during acrosome development 2. Loss of ACTL7A causes small head sperm through defective formation of the acrosome-acroplaxome-manchette complex, with mechanistic studies revealing that ACTL7A deletion impairs autophagy inhibition via the PI3K/AKT/mTOR signaling pathway, leading to PDLIM1 accumulation and manchette developmental failure 1. ACTL7A mutations are associated with Spermatogenic failure 86 and cause total fertilization failure (TFF) in 14.81% of male patients with low fertilization after ICSI 3. The protein complexes with zona pellucida binding protein (ZPBP) and regulates phospholipase C zeta 1 (PLCZ1) localization and expression, critical for calcium oscillations during oocyte activation 45. Intracytoplasmic sperm injection combined with artificial oocyte activation (ICSI-AOA) significantly rescues fertility defects caused by ACTL7A mutations, increasing fertilization rates from ~11% to ~62% 31.