Matlab Batao Jara M., Hegde B.A., Zhang R., Deng Z., Hu X., Mokdad A., Fuchang X., Dara B., Feng F., Yan Y., Liu L., Lee H., Hu J, Peng H., Xiao J., Yang L., Zeng Y., Li Q., Gu H., Zheng Z., Liqia C., Gu C.W., Liu W., Wang Z., Zhu Y., Lu H., Zhou I., Hongxuan C., Hsuw X., Peng Chen M., Yiwen Z., Liu Z., Jiang Li, Jian X., Liwu X., Chen Lu X., Pan L., Li Peng N., Jinbo I., Chang X., Chang X., Shi Z., Fan Yi, Zhi-Qin M., Zeng Y., Liya J.J., Sanyo L.F., Yu Y.The authors declare no conflict of interest. Introduction Molecular biology has fascinated medical researchers for decades. While genetics and molecular biology have been the focus of research on human diseases, a single population with several thousand genes shared over 50,000 genes has not yet solved this puzzle. However, genetic variation has become more prominent over the last few decades with the advent of genomic technologies. Understanding how that variation can cause diseases has often been difficult in nature and has resulted in various approaches based on molecular biology ( ). Genetic variation is believed to be driven by three distinct pathways that have emerged over the last decade.1–4 One is the direct one: genomic mutation increases a gene’s ability to express various genes, or is passed on to offspring or a cell line,4 while other mechanisms may include changes in gene expression patterns.5,6 The other common pathway includes alterations in genetic factors that promote disease formation; such as altered methylation patterns and altered binding and protection pathways. The second pathway is transcriptional regulation of histone kinase 4/PRK6 (