CNP and demyelinating disease: Moreover, recent studies have reported an enlarged or abnormal inner tongue in transgenic mice (e.g. 2′,3′-cyclic nucleotide 3′-phosphodiesterase (CNP)-deficient mice [23,30], in conditional knock-out of activin co-receptor Acvr1b [31] and of Pten [5] in oligodendrocytes), and in animal models of autoantibody-mediated- and cuprizone-induced-demyelinating disease [8,25], suggested to be secondary to stressed axons with a compensatory increase in need for metabolic support from the oligodendrocyte via the inner tongue.