In the Drosophila melanogaster ovary, somatic follicle cells are critical to multiple aspects of oocyte development. The specification of different sets of follicle cells establish signaling centers that not only impact the formation of the micropyle, vitelline envelope, and specific chorion structures, but also play important roles in initiation of the future A/P and D/V axes. A crucial somatic cell type, the stalk cells, form a linear structure that separates consecutive egg chambers as they are produced and continue to develop through each stage of oogenesis. Without stalk cells, egg chambers, composed of a highly organized arrangement of 16 germline cells surrounded by hundreds of specialized somatic follicle cells, can merge. Such merged or ‘fused’ egg chambers lack organization required for proper patterning and fail to produce a viable oocyte. Thus, the maintenance of stalk cells is critical for Drosophila oogenesis. We found that during normal oogenesis the stalk cells comprising a single stalk, or the connection between two egg chambers, are produced in excess and reduce in number as oogenesis proceeds and they bridge increasingly developed egg chambers. We find that this reduction arises as a result of apoptosis, a process critical in many developmental events requiring defined numbers of cells or involved in sculpting organs. Interestingly, while establishing stalks during normal development involves the eliminating of some stalk cells through apoptosis, mechanisms are clearly in place to prevent excessive loss of these cells. We have found that excessive apoptosis is prevented by JAK/STAT signaling, distinct from its proapototic role in defining exactly two polar cells at the anterior and posterior poles of each egg chamber. In addition to JAK/STAT signaling, we find that BMP signaling is also required to inhibit abnormal loss of stalk cells through apoptosis. If either JAK/STAT signaling or BMP signaling is specifically reduced in the stalk cells, we observe a more significant loss of stalk cells, such that the complete fusion of egg chambers may occur. The converse is true when JAK/STAT signaling or BMP signaling is increased. The reduced numbers of stalk cells observed when knocking down JAK/STAT signaling can be rescued through the overexpression of the BMP 5/6/7 ortholog Gbb. Similarly, the ‘long’ stalks produced by overactivation of JAK/STAT signaling can be suppressed by downregulation of gbb, supporting an intimate relationship between these two signaling pathways in defining the precise number of stalk cells that make up interfollicular stalks.