Localised mRNA translation is a widespread mechanism for targeting protein synthesis, important for cell fate, motility and pathogenesis. In Drosophila, the spatiotemporal control of gurken/TGF-α mRNA translation is required for establishing the embryonic body axes. A number of recent studies have highlighted key aspects of the mechanism of gurken mRNA translational control at the dorsoanterior corner of the mid-stage oocyte. Orb/CPEB and Wispy/GLD-2 are required for polyadenylation of gurken mRNA, but mis-localised gurken mRNA in the oocyte is not fully polyadenylated1. At the dorsoanterior corner, Orb and gurken mRNA have been shown to be enriched at the edge of Processing bodies, where translation occurs2. Over-expression of Orb in the adjacent nurse cells, where gurken mRNA is transcribed, is sufficient to cause mis-expression of Gurken protein3. In orb mutant egg chambers, reducing the activity of CK2, a Serine/Threonine protein kinase, enhances polarity defects, consistent with a phenotype relating to a mutation of a factor involved in gurken translation4. Here we show that sites phosphorylated by CK2 overlap with active Orb and with Gurken protein expression. We also consolidate the current literature into a working model for gurken mRNA translational control and review the role of kinases, cell cycle factors and polyadenylation machinery highlighting a multitude of conserved factors and mechanisms in the Drosophila egg chamber.