This is unlikely to be the case for the majority of cancers where mutations of FGFR3 are rare (Intini et al, 2001; Karoui et al, 2001; Sibley et al, 2001), although FGFR3 may be inactivated by aberrant-splicing and activation of cryptic splice donor sites (Jang et al, 2000). Here, FGFR3 is linked to cancer.