In this context, it has been reported that T3 are capable to correct aberrant splicing of IkappaB kinase complex-associated protein (IKAP) in cells derived from patients with familial dysautonomia [2] and to modulate the expression of a specific set of miRNAs in HeLa cells involved in the alternative splicing of pro-apoptotic proteins, such as the X-box binding protein 1 (XBP-1) [10]. The gene discussed is XBP1; the disease is Riley-Day syndrome.