DACH1 and neoplasm: Surprisingly, these inhibitors also exhibited low levels in the F2↑ tumor, and we hypothesize that their lack is linked to the presence of degradation signals in the FGFR C-terminus [5, 27] and absence of constitutive dimerization provided by the TACC domain [10, 66], perhaps allowing overexpressed FGFR2 a more physiological signaling controlled by strong negative feedbacks, possibly mediated by DACH1 [33, 34] (Fig. 5d).