The human epidermal growth factor‐receptor (EGF‐R) was introduced into primary mouse bone marrow cells (BMC), utilizing retrovirus mediated gene transfer. Cultivation of infected BMC in the presence of interleukin‐3 (IL‐3) led to the outgrowth of IL‐3 dependent myeloid cells, which efficiently expressed functional EGF‐R, exhibiting its two characteristic affinity states. EGF acts on these cells synergistically with IL‐3 in stimulating DNA synthesis and cell proliferation even under IL‐3 saturation conditions. However, EGF was not sufficient to replace the requirement for IL‐3. In contrast, EGF was able to maintain proliferation of a factor‐dependent hemopoietic cell line (FDC‐P1) infected with the EGF‐R retrovirus in the absence of IL‐3, but these cells did not respond to EGF in the presence of IL‐3. No influence of EGF on IL‐3 induced mast cell differentiation of BMC expressing the EGF‐R could be observed by histological criteria. These data show that the expression of EGF‐R alone is not sufficient to induce or maintain cell proliferation in IL‐3 dependent bone marrow derived cells, although it can do so in established hemopoietic cell lines.