Jianfei Qi has written:

'Role of N-cadherin and beta-catenin signaling during transendothelial migration of melanoma cells'

RET protooncogene mutation which encodes a transmembrane receptor with tyrosine kinase activity has been linked to PTC and activating mutation of BRAF Activating point mutations in the RAS oncogene has been found in patients with follicular adenoma and carcinoma and p53 mutation and PAX8-peroxisome proliferator-activated receptor gamma [PPAR γ1] and PIK3CA mutations and amplifications and PTEN mutations in the PI3K/Akt signaling pathway and beta-catenin mutations

The correct answer would be because of a protein known as dickkopf 1, or DKK1.

Investigators looked at the dermis, the layer on the skin beneath the epidermis (outer layer), and a certain type of cell within this layer, called a fibroblast. They found that the fibroblasts in the soles and palms secrete higher levels of a protein known as dickkopf 1, or DKK1, than the fibroblasts in the dermis at other body sites. It is believed that the rich source of DKK1 in these areas affects the epidermal layer above it and creates the physical characteristics of thickened, paler skin.

DKK1 reduces skin pigmentation by suppressing the development and action of pigment producing skin cells called melanocytes. It also reduces the transportation of this pigment from melanocytes to the target skin cells for melanin (keratinocytes).

DKK1 also thickens the epidermis by increasing the number of skin cells and their density. Three genes affected by DKK1 - keratin 9, αKLEIP and β-catenin - have been found to cause this thickening. Keratin 9 reinforces the skin against physical impact, αKLEIP aids in cell division (multiplying) and makes cells smaller and, finally, a reduction in β-catenin is also possibly involved in cell contraction (making the cells more compact).