“…Multiple FGFs can activate both FGFR2 IIIb (FGF3, 7, and 22 from the Fgf7 subfamily; but also FGF1) and FGFR2 IIIc (e.g., FGF1, 2, 4, 5, 6, 8, 9, or 16) ( Zhang et al, 2006 ). Nevertheless, the Fgf10 and Fgfr2 null mice share the majority of defects within the orofacial area, with the exception of milder tooth and inner ear defects in Fgf10 mutant mice ( Kettunen et al, 2000 ; Ohuchi et al, 2000 ; Pirvola et al, 2000 ), and development of medial nasal glands, which are absent in Fgfr2 null mutants but form normally in Fgf10 null mice ( May et al, 2016 ). The milder phenotypes in Fgf10 mutants are mostly explained by compensation by FGF3 ( Kettunen et al, 2000 ; Wright, 2003 ) or FGF7 ( May et al, 2016 ).…”