The rationale of this study is based on our data that (1) in human PAD muscle biopsies increased VEGF165b binding to VEGFR2 correlated with increased VEGFR2 activation, whereas increased VEGF165b binding to VEGFR1 correlated with decreased VEGFR1 activation vs. non-PAD controls, and (2) in in vitro competition studies, exogenous VEGF165b-induced VEGFR2 activation almost to the same extent as VEGF165a in ECs and (3) VEGF165b inhibition-induced VEGFR1 activation without changes in VEGFR2 activation [8]. This evidence concerns the gene FLT1 and peripheral arterial disease.