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, approximately half the cases of autosomal recessive non-syndromic hearing loss and a significant proportion of sporadic hearing loss can be linked to mutation in the gene encoding connexin 26.