DNA interstrand crosslinks (ICLs), created by chemotherapeutic agents and endogenous agents like metabolic by-products, inhibit DNA replication and transcription. Removal of these ICLs is critical for restoring normal DNA metabolism and maintaining genomic integrity. The proteins in the Fanconi anaemia pathway orchestrate the various steps involved in the ICL repair. So far, 22 proteins have been found to be involved in this pathway, and mutations in any one of the genes which code these proteins cause impaired ICL-repair and Fanconi anemia (FA), the most common inherited bone marrow failure disease in humans. FA cells are characterized by their hypersensitivity to endogenous and exogenous DNA crosslinking agents, their spontaneous chromosomal instability, G2/M cell cycle arrest, and reduced cell survival. Bone marrow failure is the major cause of mortality in FA patients, and genomic instability in FA causes clonal evolution and tumour progression. Previously, we have carried out genome analysis of the FA patients and generated FA-induced pluripotent stem cells (iPSCs). In this project, by genomic, transcriptomic and proteomic analyses of FA cells and disease modelling using iPSCs, we plan to understand the molecular basis of this disease.