Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults. AML is a heterogeneous disease that results from genetic alterations in normal hematopoietic stem cells. These alterations induce an arrest of differentiation and/or excessive proliferation of abnormal leukemic cells or blasts [1]. Recent genomic studies have identified that recurrent somatic mutations in AML patients block differentiation and/or enhance self-renewal by altered transcription factors (2,3). Genetic or epigenetic changes acquired by AML cells disrupt key growth regulatory pathways and the changes will cause normal cells to achieve certain malignant characteristics, including inappropriate proliferation in the absence of normal growth signals, self-renewal undefined in a stem cell-like manner, evasion of programmed cell death, inhibition of differentiation, aberrant cell cycle checkpoint control, and genomic instability [4]. Incidence and Prevalence AML is the most common form of acute leukemia in adults and accounts for the largest number of annual leukemia deaths in the United States, with approximately 18,860 new cases and 10,460 deaths expected in 2014 (Cancer Facts & Figures 2014). In the Indian scenario, although there is not much published data on the incidence and prevalence of AML, it is worth noting that the median age of diagnosis of AML is much lower than that of Western population. The median age of the Indian population is between 41 and 45 years (Phillip et al, unpublished data, CMC, Vellore, Dunna, Rajappa et al. 2010, Abraham, Varatharajan et al. 2012).EtiologyMost cases of AML are sporadic, characterized by the acquisition of somatic mutations in hematopoietic progenitors that confer proliferative activity...... middle of article ......es the anti-leukemic activity of Ara- C [27]. Ribonucleotide reductase (RR) De novo nucleotide biosynthesis pathway There is shown to interact with the Ara-C activation pathway via the enzyme ribonucleotide reductase (RR). RR-generated dNTPs act as a competitive inhibitor against the active metabolite Ara-CTP and prevent them from incorporating into DNA. Additionally, elevated intracellular pools of dNTPs inhibit dCK activity, thereby reducing Ara-C activation. The RR holoenzyme is a dimeric protein and comprises large and small subunits, ribonucleotide reductase M1 (RRM1) and ribonucleotide reductase M2 (RRM2). In patients with advanced non-small cell lung cancer treated with gemcitabine, a drug with a metabolic pathway similar to that of Ara-C, low levels of RRM1 mRNA expression were associated with to a significantly longer median survival than those with high levels. [28] [29].