TBX1 and 22q11.2 deletion syndrome: Instead, 22q11DS phenotypes may result from altered neural crest-mediated interactions with mesodermal or endodermal targets that express Tbx1. Our evidence suggest that a significant portion of the 22q11DS phenotypic spectrum reflects the coordinated expression of multiple 22q11 genes and their dosage-sensitive influence on neural crest-mediated M/E induction beyond that of Tbx1 (Maynard et al., 2013, 2020a; Karpinski et al., 2014; Motahari et al., 2020).