FGFR3 and neurofibromatosis type 1: More in general, the whole mutational landscape of the Neurofibromatosis type I patients appears related to the gene context and length, differently from other examples of constitutional variability, like FGFR3 or FGFR2, which show hotspots, a single mutational mechanism causing a gain‐of‐function and a clear correlation to the paternal age, consistent with the increased number of cell divisions occurring in aging spermatogonia.38