We investigated the relationship between eight polymorphisms in the gene encoding for vascular endothelial growth factor (VEGF) (−1540C > A, −1512Ins18, −1451C > T, −460T > C, −160C > T, −152G > A, −116G > A and +405G > C) and plaque-type psoriasis stratified for age at onset, gender and family history of dermatosis. For this purpose, 117 patients with chronic plaque-type psoriasis and 215 healthy subjects were enrolled. We found that being homozygous −1540AA, −1512InsIns, −1451TT, −460CC and −152AA conferred a significant risk in developing psoriasis compared with heterozygous (−1540CA, −1512 + Ins, −1451CT, −460CT and −152AG) and homozygous genotypes (−1540CC, −1512 + +−1451CC, −460TT and −152GG) grouped together [odds ratio (ORs) = 1.73, 1.73, 1.73, 1.77 and 1.87, respectively]. Conversely, having the −116AA or +405GG genotype did not significantly increase the risk of disease expression compared with other genotypes of the same loci. Interestingly, we found that −1540AA, −1512InsIns, −1451TT, −460CC and −152AA homozygous genotypes have a significant two-fold increased risk in developing psoriasis after the age of 40 years (late-onset psoriasis) (ORs = 2.19, 2.19, 2.19, 2.05 and 2.26; P = 0.02, 0.02, 0.02, 0.04 and 0.02, respectively) as compared with controls. On the contrary, we found no phenotype–genotype association of the same magnitude among the patients in whom psoriasis developed at or before the age of 40 years (early-onset psoriasis) compared with controls. Genotype distributions were not significantly different when cases and controls were stratified either by gender or family history of psoriasis. Finally, VEGF plasma concentration was not significantly different between patients and controls and was not correlated with the severity of the disease.