Our lead product candidate represents a fundamentally differentiated therapeutic strategy, designed to directly correct the underlying beta-globin gene mutation in hematopoietic stem cells (HSCs) of patients with sickle cell disease (SCD), thereby restoring normal adult hemoglobin (HbA) expression and offering a corrective true cure. Unlike alternative approaches that merely boost fetal hemoglobin (HbF) levels, true gene correction addresses the root cause of SCD by diminishing sickle hemoglobin (HbS) production because of true gene correction, avoiding the persistent risks associated with incomplete disease modification. In SCD, a single point mutation in the beta-globin gene of HSCs leads to the production of HbS in mature red blood cells (RBCs) instead of functional HbA. This disrupts normal hemoglobin interactions, causing HbS proteins to polymerize into insoluble chains that deform RBCs into rigid, sickle-shaped structures. These dysfunctional cells impair oxygen transport, obstruct blood flow, and trigger severe symptoms including chronic pain, hemolytic anemia, and organ damage. While HbF-boosting therapies can mitigate most vaso-occlusive events by inhibiting HbS polymerization, they fall short of full disease resolution. The presence of HbS, even with protective factors like elevated HbF, does not eliminate long-term clinical risks. By contrast, Kamau’s precision editing platform aims to convert HbS to HbA at high efficiency, potentially eradicating these complications and delivering superior and durable outcomes for patients.