The esophageal squamous cell carcinoma (ESCC) is thought to develop through a multi-stage process.Epigenetic gene silencing constitutes an alternative or complementary mechanism to mutational eventsin tumorigenesis. Posttranscriptional regulation of human leukocyte antigen class I (HLA-I) and antigenprocessing machinery (APM) proteins expression may be associated with novel epigenetic modifications incancer development. In the present study, we determined the expression levels of HLA-I antigen and APMcomponents by immunohistochemistry. Then by a bisulfite-sequencing PCR (BSP) approach, we identified targetCpG islands methylated at the gene promoter region of APM family genes in a ESCC cell line (ECa109), andfurther quantitative analysis of CpG site specific methylation of these genes in cases of Kazakh primary ESCCswith corresponding non-cancerous esophageal tissues using the Sequenom MassARRAY platform. Here weshowed that the development of ESCCs was accompanied by partial or total loss of protein expression of HLA-B,TAP2, LMP7, tapasin and ERp57. The results demonstrated that although no statistical significance was foundof global target CpG fragment methylation level sof HLA-B, TAP2, tapasin and ERp57 genes between ESCCand corresponding non-cancerous esophageal tissues, there was significant differences in the methylation levelof several single sites between the two groups. Of thesse only the global methylation level of LMP7 gene targetfragments was statistically higher (0.0517±0.0357) in Kazakh esophageal cancer than in neighboring normaltissues (0.0380±0.0214, p<0.05). Our results suggest that multiple CpG sites, but not methylation of every siteleads to down regulation or deletion of gene expression. Only some of them result in genetic transcription,and silencing of HLA-B, ERp57, and LMP7 expression through hypermethylation of the promoters or othermechanisms may contribute to mechanisms of tumor escape from immune surveillance in Kazakh esophagealcarcinogenesis.