This result suggested that under different physiologic or pathologic conditions, specific PG species can exert opposite effects to “normalize” keratinocyte proliferation, although the current THZ1 report suggests that this normalization reflects, at least in part the presence in egg PG of more than one PG species with different signaling functions. Although synthetic polyunsaturated fatty acid-containing PGs, and in particular DLPG, seemed most effective at inhibiting keratinocyte proliferation in vitro, the expense of these PGs could potentally preclude their use as a treatment for psoriasis. Therefore, we also investigated the ability of soy PG, a mixture of PG species containing a high proportion of polyunsaturated fatty acids, to inhibit keratinocyte proliferation. This lipid also has the advantage of being a natural product, and our results in vitro indicated its efficacy. Previously, we had also shown that neither DOPP nor DPPP altered keratinocyte proliferation ; however, the corresponding PG species either tended to stimulate keratinocyte proliferation or significantly stimulated keratinocyte proliferation. Likewise, although both DLPG and DLPP inhibited keratinocyte proliferation, the effect of DLPG was significantly greater than that of DLPP. Together these results indicate the importance of the head group in determining the effects of PG and argue against the idea that the fatty acids are being released from the PG phospholipid to induce the disparate effects observed. Several questions remain. For example, what downstream targets of the specific PG species exert the inhibitory or stimulatory effects on keratinocyte proliferation? We speculate that PG exerts different effects through different effector pathways. One potential mechanism stems from the observation by Murray and Fields that in human leukemia cells PG binds to and stimulates protein kinase C?II, an Acrivastine important protein kinase mediating proliferation in these cells. Furthermore, these authors demonstrated that specific PG species exhibit different activities but that other phospholipids do not mimic the effect of PG, suggesting that the ability of PG to activate PKC?II resides in the head group.