In 2012, Lin et al. (2012) found that gain-of-function mutations in TRPV3 (p.Gly573Cys, p.Gly573Ser, and p.Trp692Gly) lead to sustained channel opening, continuous influx of Ca2+ into cells, causing calcium overload and inducing increased apoptosis of keratinocytes, which may result in the hyperkeratosis observed in OS. Here, TRPV3 is linked to Hyperkeratosis.