An absence of typical SFD-related pathology in the mutant mice such as thickening of Bruch’s membrane, atrophy of the choriocapillaris and spontaneous CNV, and significant increases of pro-angiogenic proteins seen in cultured cells like upregulation of VEGFR-2 and bFGF levels lead one to speculate that either the short life span of the mouse may not allow sufficient accumulation of the protein to generate pathology or transgenic mice adapt to molecular or functional changes via a compensatory mechanism. Here, KDR is linked to Sorsby fundus dystrophy.