Eccentricity of the proteins implicated in cell cycle checkpoints is awfully common among almost all cancers including lung cancer. The grail of the present study was to inquest the role of codon 109 of p27KIP1 and codon 148 of p16INK4A polymorphism as susceptible cell cycle regulator and to harmonize between genetic polymorphism and risk factors of lung cancer in a Bangladeshi population. Two hundred subjects were selected to explore single nucleotide polymorphisms of allelic variants of selective genes using Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCRRFLP). Risk of lung cancer was reckoned as odds ratio (OR) at 95% confidence interval (CI) using logistic regression models adjusting for age, sex, and tobacco use. The frequency of Val/Gly heterozygosity of codon 109 was found to be significantly associated with lung cancer (OR= 3.38, 95% CI= 1.64-6.96, p= 0.0010). In contrary, both heterozygous Ala/Thr and mutant Thr/Thr form of codon 148 were significantly linked with lung cancer risk (OR= 3.86, 95% CI= 1.45 to 10.23, p= 0.0067; OR= 3.86, 95% CI= 1.19 to 12.48, p= 0.0242, respectively). Also inconsequential association was found between smoking and polymorphism of codon 109 of p27KIP1, codon 148 of p16INK4A. Accordingly present findings propound that both codon 109 of p27KIP1 and codon 148 of p16INK4A may contribute to susceptibility of lung cancer in a Bangladeshi population