Interestingly, point mutations in humans that disrupt GATA-1/FOG-1 interaction are associated with familial dyserythropoietic anemia and thrombocytopenia [15], and a point mutation in GATA-1 that inhibits FOG-1 binding cannot rescue erythroid differentiation in a GATA-1 deficient cell line. The gene discussed is GATA1; the disease is Anemia of inadequate production.