For example, desquamation occurs more slowly at acral (palm and sole) surfaces and more rapidly where the skin is thin, such as the eyelids.

[3] Kallikreins are serine proteases; packaged within the lamellar bodies and released into the intercellular space between the keratinocytes as they transition into becoming corneocytes.

[3] Slowing the process of corneocyte desquamation allows acral (palm and sole) skin to form a thick protective stratum corneum.

In pathologic desquamation, such as that seen in X-linked ichthyosis, the stratum corneum becomes thicker (hyperkeratosis), imparting a "dry" or scaly appearance to the skin, and instead of detaching as single cells, corneocytes are shed in clusters, which forms visible scales.

Toxic shock syndrome, a potentially fatal immune system reaction to a bacterial infection such as Staphylococcus aureus,[4] can cause severe desquamation; so can mercury poisoning.

Other serious skin diseases involving extreme desquamation include Stevens–Johnson syndrome and toxic epidermal necrolysis (TEN).