Background:5-fluorouracil(5-FU) has been extensively used as monotherapy or in combination therapy for a variety of solid cancers. Capecitabine, a novel oral fluoropyrimidine derivative may be converted to 5-FU selectively in tumors. Although treatment with 5-FU is generally well tolerated, few people often experience fluoropyrimidine-related toxicity. This can be explained by clinical factors. However, much variability in toxicity remains unexplained. Dihydropyrimidine dehydrogenase (DPYD) is a rate limiting metabolizing enzyme for fluorouracil and its prodrug capecitabine. Reports show that G>A single nucleotide polymorphism at the 5’-splice sequence of exon 14 (DPYD*2A) of DPYD gene to be highly polymorphic, which leads to the formation of a truncated non-functional protein. It is considered to be predictive marker as about 50% DPYD*2A allele carriers actually develop severe toxicities with 5-FU. However, the polymorphism pattern of DPYD*9 and DPYD*2 and its association with tolerability are limited in Indian setting. In silico analysis of the SNPs using bioinformatics tools, SIFT, Polyphen 2 and I Mutant 3 showed that all the four SNPs were deleterious. Hence selection of these SNPs is justifiable.