Cone cornea is a progressive, non-inflammatory corneal disease that causes corneal thinning and irregularity, and consequently impaired vision. It usually begins in adolescence and progresses slowly through young adulthood and middle age. Some children have a more rapid progression of cone corneas. In the last 5-10 years, corneal collagen cross-linking has become a promising treatment. Patients with mild cone corneas should be treated early to achieve more benefit, rather than waiting until they are older and the disease has progressed. A prospective study by Vinciguerra and colleagues, published in Am J Ophthalmol, Italy, studied 40 children, ages 9-18 years (mean 14.2 years), who were considered to have progressive moderate cone corneas. Progression in this study was defined as: An increase in myopia or astigmatism of at least 3D within the past 3 months An increase in mean central corneal curvature of at least 1.5D on topography within the past 3 months A decrease in mean central corneal thickness of at least 5% on 3 consecutive tests of corneal topography within the past 3 months The thinnest portion of the cornea was at least 400 μm thick. Standard de-epithelialization cross-linking was performed under local anesthesia using riboflavin for 30 minutes. Postoperative follow-up showed a significant improvement in both bare eye visual acuity and best-corrected visual acuity with lenses (P<0.05). The mean equivalent spherical refraction decreased by approximately 1.57 D at 24 months (P=0.02). Both mean corneal flat K and steep K values decreased. mean central corneal thickness decreased significantly at 6 months (P=0.04) and gradually recovered at 12 months. Endothelial cell count did not change significantly (P=0.32). Perspective: Weakening of the corneal stroma causes the cornea to thin or protrude, forming a cone cornea and affecting vision. Why this happens is not yet known. The discovery that the cornea can be strengthened by increasing molecular bonds led to collagen cross-linking as a treatment for cone corneas. By saturating the corneal stroma with riboflavin and activating it with A-band UV light, the released free radicals induce increased covalent bonding between collagen proteins. Many studies have confirmed that there is a short or medium term arrest of disease progression, often accompanied by corneal flattening and corneal regularity improvement. There are many studies on adults in this area. Since the "proof of concept trial" established that corneal collagen cross-linking has a good safety profile (short and intermediate term) for slowing or halting conical cornea progression, the next step in testing in the pediatric setting is reasonable. The 2-year results are very encouraging. Not only did the conical cornea no longer progress, but all corneal parameters improved significantly. Corneal thickness decreased at 6 months, but returned to baseline at 1 year and stabilized at 2 years. And there were no major adverse events. However this is only a 2-year study and these children will need to use their corneas for many more years. At this point, it seems quite reasonable to treat rapidly progressing cone corneas with corneal collagen cross-linking. The next question is whether it is possible to treat eyes that have not yet proven to be progressive cone corneas in advance of disease progression. This requires more long-term follow-up to prove its effectiveness and safety.