LSS (lanosterol synthase) is a key enzyme in cholesterol biosynthesis that catalyzes the cyclization of (S)-2,3 oxidosqualene to lanosterol, forming the sterol nucleus 1. This amphipathic molecule lanosterol is enriched in the lens and plays a crucial role in preventing protein aggregation and maintaining lens transparency 1. The mechanism involves lanosterol's ability to prevent disruption of crystallin protein interactions, thereby maintaining the highly ordered macro-structure essential for lens function 1. LSS mutations have significant disease relevance, as homozygous missense mutations (W581R and G588S) in LSS cause congenital cataracts by impairing the enzyme's catalytic function 1. Additionally, LSS variants are associated with hypotrichosis 14, a form of congenital alopecia, with novel variants recently identified in Chinese families including deletions and missense mutations 2. The gene is also linked to alopecia-intellectual disability syndrome 4 (APMR4), with patients showing variable degrees of intellectual disability, alopecia, and additional phenotypic features 3. Clinically, lanosterol treatment has shown promise in reducing protein aggregates in vitro and decreasing cataract severity in animal models, suggesting potential therapeutic applications for cataract prevention and treatment 1.