FGFR1 and Kallmann syndrome: Altogether, in our search we identified seven FGFR1 mutations that have been proposed as causative in seven patients with Kallmann syndrome, exhibiting CL/P and TA among other main phenotypes (Supplementary Table 4) (Zenaty et al. 2006; Xu et al. 2007, 2015; Bailleul-Forestier et al. 2010; Tommiska et al. 2014), representing relevant insights into a possible common FGFR1-related mechanism that may contribute to the dual etiology of OFCs and TA.