Based on limited published evidence, CCNYL1 is a key regulator of Wnt signaling implicated in male fertility, embryonic neurogenesis, and cortex development. It activates cyclin-dependent kinase CDK16 and promotes sperm maturation and flagellated sperm motility. A genome-wide association study identified CCNYL1 as a thyroid-dysgenesis risk locus at 2q33.3, with increased thyroidal expression associated with perturbed Wnt signaling in thyroid development 1. Additionally, CCNYL1 was identified as a causal factor in histone deacetylase inhibitor-induced cell death in cancer models 2.