Sea urchin embryos show a great affinity to replace cells necessary for normal development through a process called transfating in which cells in the embryo express genes of other cells to compensate for the removal. Specifically, the removal of primary mesenchyme cells (PMCs) which are crucial to the development of the skeleton triggers non-skeletogenic mesoderm (NSM) cells to reprogram in order to express genes found in the PMC gene regulatory network (GRN). A possible explanation is that the PMCs provide a signal to the surrounding NSMs that inhibit NSM transfating. This study seeks to determine 1) which genes are expressed in the PMCs and 2) what signal the PMCs provide to inhibit NSM transfating. Through in situ hybridization experiments using newly synthesized probes from a candidate gene list, we hope to determine which genes are PMC specific. Using in situ hybridization and drug inhibitor treatments, we test for ectopic cell reprogramming in order to determine the specific signaling molecules from the PMCs to inhibit NSM transfating. This study can broaden our understanding of the signaling molecules crucial to normal sea urchin development.