Each of the approximately 20 connexin isoforms produces channels with distinct permeabilities and electrical and chemical sensitivities; therefore, one connexin usually cannot fully substitute for another. Consequently, a wide variety of malignant phenotypes associate with decreased connexin expression and gap junction communication, dependent on the particular connexin that is effected. For instance, mutations in connexin 32 result in Charcot-Marie-Tooth disease, a demyelinating disease of the peripheral nervous system.