The connexin family of mammalian gap junction proteins provides intercellular communication channels critical for development and tissue function. Mutations in connexins are associated with numerous diseases including deafness, skin diseases, cataracts, cardiac diseases, neurological diseases, cancer, and complex syndromic disorders. Connexin 43 (Cx43, encoded by GJA1) is the most widely expressed and studied member. We and others have shown that, through a poorly understood mechanism of direct internal translation initiation, the single coding exon of GJA1 generates various N-terminally truncated Cx43 forms, notably the 20 kDa (k) form GJA1-20k.1,2 Numerous functions have subsequently been ascribed to these truncated forms, providing critical insight into non-canonical GJA1 functions.3