Steroid receptors transcribe genes that lead to important biological processes, including normal organ development and function, tissue differentiation, and promotion of oncogenic transformation. These actions mainly result from nuclear steroid receptor action. However, for 50 years it has been known that rapid effects of steroid hormones occur and could result from rapid signal transduction. Examples of these effects include stress responses to secreted glucocorticoids, rapid actions of thyroid hormones in the heart, and acute uterine/vaginal responses to injected estrogen. These types of responses have increasingly been attributed to rapid signaling by steroid hormones, upon engaging binding proteins most often at the cell surface of target organs. It is clear that rapid signal transduction serves an integrated role to modify existing proteins, altering their structure and activity, and to modulate gene transcription, often through collaboration with the nuclear pool of steroid receptors. The biological outcomes of steroid hormone actions thus reflect input from various cellular pools, co-coordinating the necessary events that are restrained in temporal and kinetic fashion. Here I describe the current understanding of rapid steroid signaling that is now appreciated to extend to virtually all members of this family of hormones and their receptors.