These findings suggest that cysteine residues may have a critical function in suspensory ligaments of the eyes and led to the speculation that the pathophysiology of ectopia lentis is related to a disruption of the structural function of fibrillin-1 in the 10–12 nm extracellular microfibrils in the ciliary zonule [14,27]. This evidence concerns the gene FBN1 and isolated ectopia lentis.