The aim of this paper is to set forth a new concept of human sebaceous gland functioning and to examine certain forces influential in the gland's activityf. In essence, the current view is that the sebum which accumulates on the surface is the chief force regulating the gland's excretory activity. This theory, first proposed by Schur and Goidfarb (2) and subsequently elaborated speculatively by Emanuel (3), states that the gland starts to excrete sebum immediately upon removal of the surface lipoids. This process is at first rapid, but progressively slows down as more and more surface sebum accumulates, finally reaching a standstill when the lipoid layer is completely replaced. The curve of replacement rises sharply at first and then levels off, defining an asymptotic hyperbola (4). The classical interpretation is that the surface layer of sebum finally reaches a height sufficient to counteract the excretory force of the gland, causing the gland to shut down. Emanuel (3) emphasizes that the consistency of the sebum significantly influences the final height of the lipoid layer which will cause standstill: the more viscous the sebum, the thinner the layer. Butcher's (5) physical measurements of sebum seem to sustain this fully. Sebum cools as it approaches the surface tending to solidify at or near the surface temperature (30°C) at which point its viscosity increases abruptly. Butcher accordingly endorses Emanuel's views. The experimental foundation of Schur and Goldfarb's f In view of the profound differences between human and animal skin, we have elected to exclude from consideration knowledge obtained from animal experimentation. The periodic wave-like changes which envelop the skin of those animals which have been most studied (rats, mice, hamsters), are lacking in humans. As part of the animal “skin cycle” the sebaceous gland enlarges, fills and disgorges periodically, a phenomenon which has no parallel in humans (1).