Hemopoietic stem cell differentiation represents the primary rule of self-renewal, proliferation, and specialization modulated by several mechanisms, including growth factors, cell interactions, and bioavailability of various ions, especially Ca²⁺ and Zn²⁺. Apoptotic death, during normal cell turnover, has been widely studied and is recognized as an important pathway for clonal deletion in the hemopoietic system. Multi-parametric analyses have shown that subjects with Down syndrome show low levels of plasmic zinc associated with the presence of immature myeloid cells in the peripheral blood. This arrangement is repaired by in vivo zinc therapy. This study presents morphological and biochemical analyses to show that ZnSO₄ therapy induces the disappearance of peripheral myeloid precursor cells by a programmed cell death mechanism. The programmed zinc-therapy-induced cell death presumably provides a simple way to regulate the myeloid differentiation selecting appropriate cells.