Background • The chronic lymphocytic leukemia (CLL) pathogenesis shows a molecularly variable disease with particular cytogenetic characteristics that constitute nowadays the major prognostic factors. • The epidemiology of CLL in the Middle Eastern population has not been fully studied. • The modeling of the CLL epidemiology at the population level is required to personalize the treatment plan at the individual level. Patients & methods • All the newly diagnosed CLL patients who did not require treatment were eligible. • Patients were investigated for demographic characteristics and CLL testing by cytogenetics and FISH. Results • Chromosomal aberrations on classical karyotype were found 53.6% among which 26.7% present complex rearrangements. • The most frequent abnormality in all patients was del(13q14) [46.4%] occurring as a sole abnormality in ten cases. • FISH studies identified ch14q32 rearrangement (25.0%), followed by trisomy 12 (14.3%), del(17p13) and del(11q22) in 7.1% each. Discussion • Similar to large studies from both Western and Eastern countries, del(13q14) was the most common abnormality in CLL patients. • It is rational to encounter low incidence of poor prognosis FISH abnormalities in our watch and wait CLL patients. Conclusion • The higher prevalence of del(13q14) as a sole abnormality could be the primary event in inducing CLL. • The del(17p13) and del(11q22) follow and could be drivers for CLL progression. Aim: We aimed to understand the biology of chronic lymphocytic leukemia (CLL) patients in Lebanon. Materials & methods: We applied conventional cytogenetic and FISH studies on Lebanese patients diagnosed with CLL and undergoing a watch and wait approach. Results: Our study disclosed 53.6% of patients with aberrant karyotypes among which 26.7% were complex karyotypes. Genetic aberrations included del(13q14) 46.4%, 14q32 translocation in 25%, trisomy 12 in 14.3%, del(17p13) and del(11q22) in 7.1% each. The deletion of 6q21/6q23 was not found in any of our patients. Conclusion: The higher prevalence of del(13q14) as a sole abnormality could be the primary event in inducing CLL. The del(17p13) and del(11q22) followed as potential drivers for progression in CLL patients with a watch and wait approach.