I was involved in my master thesis with the topic Evaluation of Cyclin D1 and H-Ras gene expression patterns in leukemic blood samples using Real-Time PCR at the Regional Cancer Center, Trivandrum, India. This thesis mainly focuses on the signalling pathway, via c-myc/MAP kinase, resulting in the overexpression of cyclin D1 and H-Ras. While doing my research thesis, I found that in most of the Chronic Myeloid Leukemia (CML) cases, there is an overexpression of cyclin D1, the reason for the unregulated proliferation of cells from G1 to S phase. Similarly, H-Ras, too, is found to be over expressed in most of the CML cases, indicating that the cyclin D1 over expression is as a result due to the H-Ras, c-myc/MAP kinase pathway. Meanwhile, after reading research articles/journals on CML, I learnt that there are other pathways and may be interacting as well, in a complex web that influences the cyclin D1 expression pattern. Samples (5ml of blood or bone marrow) were collected in heparinized vials, mononuclear cells were isolated, using the standard procedure, and stored in RNase later solution at -20 degree Celsius until isolation of RNA.RNA from the samples were disjunct using procedure supplied in the kit. After disjunction (of RNA), analysis of the integrity of RNA was performed on 1% agarose gel and observed under the gel dock The quality of RNA was analyzed by comparing the intensity of 28s and 18s rRNA. Concentration and purity of RNA were also determined using spectrophotometry. After analysis of RNA, construction of cDNA was performed using polymerase chain reaction (PCR). After this step, Cyclin D1 and H-Ras expression were analyzed using Real-Time Polymerase Chain Reaction (RT-PCR). I also studied blood samples of treated CML patients. In this result, I found that the cyclin D1 is still overexpressed but H-Ras expression is found to be normal in most of the samples. This result raises questions like has cyclin D1 acquired any resistance against targeted therapy?