Specifically, Cyp26b1, encoding an RA degradation enzyme, Zbtb16, an undifferentiated spermatogonia marker gene, and Smcp (Sperm mitochondria-associated cysteine-rich protein), its loss causing asthenozoospermia [48], all lost their rhythmicity in the desynchronization group (Fig. 7i–k), implicating that circadian desynchronization likely leads to dysregulated RA signaling and defects in spermatogenesis and fertilization in mice. This evidence concerns the gene CYP26B1 and Reduced sperm motility.