The discovery of new inherited bone marrow failure syndromes (IBMFSs) has expanded the diagnostic landscape of cytopenic disorders beyond classical entities like Fanconi anemia and dyskeratosis congenita. Advancements in genomic technologies, particularly next-generation sequencing (NGS), have identified novel syndromes associated with mutations in genes such as Myb-like SWIRM and MPN domains (MYSM1), ERCC6L2, MECOM, sterile alpha motif domain–containing (SAMD9/SAMD9-like (SAMD9L)) genes, DNAJC21, alcohol dehydrogenase 5 (ADH5)/aldehyde dehydrogenase 2 (ALDH2), TP53, MDM4, and oncostatin M (OSM). These disorders typically present with early-onset cytopenias, syndromic features, and a variable but often high risk of progression to myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). Unique mechanisms include somatic genetic rescue (SGR), digenic inheritance, ribosomopathies, and gain-of-function (GOF) TP53 activation. Clinical phenotypes range from isolated marrow failure to multisystem syndromes with neurodevelopmental, skeletal, endocrine, and immunologic involvement. Hematopoietic stem cell transplantation remains the only curative treatment for many, although precise timing is critical. This chapter reviews the genetic underpinnings, clinical features, diagnostic strategies, and therapeutic considerations for these emerging IBMFSs, offering insights for early identification and personalized management.