<p>N⁶-methyladenosine (m⁶A), the most prevalent epitranscriptomic modification in eukaryotic mRNA, dynamically regulates mRNA stability, splicing, and translational efficiency through a sophisticated “writer-eraser-reader” network. This system comprises methyltransferase writers (e.g., METTL3/14, METTL16, WTAP), demethylase erasers (e.g., ALKBH5, FTO), and recognition readers (e.g., YTHDC2, YTHDF2, hnRNPC). This precise regulatory mechanism governs spermatogonial stem cell proliferation, meiotic initiation, and spermatid maturation by orchestrating cell cycle progression, meiotic timing, and sperm morphological functionality. The depth and breadth of its regulation are further demonstrated via deep integration with related signaling pathways, as it collaboratively regulates the PI3K/AKT/mTOR pathway that maintains the metabolic homeostasis of spermatogonial stem cells, the Wnt/β-catenin pathway that coordinates stem cell renewal and meiotic initiation, the GnRH pathway that connects neuroendocrine regulation, and the ERK1/2 pathway that mediates key events of cell proliferation and differentiation. This multipathway synergy jointly ensures the normal progression of spermatogenesis. Furthermore, an interplay exists between m⁶A modification and ubiquitination modification. While m⁶A regulates the expression of genes related to ubiquitination by influencing the protein degradation pathway, ubiquitination regulates the methylation of m⁶A either by directly modifying m⁶A or by participating in the activity of related enzymes indirectly. This review provides a novel perspective for understanding the epigenetic mechanisms of spermatogenesis and discusses intervention strategies for managing male infertility by systematically integrating the dynamic distribution of m⁶A, its core regulatory mechanisms, and its interaction with multidimensional signaling networks.</p>