What you might have read described as "silencing the alarm" has a clinical name: tachyphylaxis. Your dermatologist almost certainly knows about it. Most never bring it up.
The cream suppresses inflammation. That part works. It always has.
But inflammation isn't the same thing as the structure that's breaking down. Your skin barrier is a separate layer — the lipids between your skin cells, built from ceramides, oleic acid, and palmitic acid. The cream doesn't touch it.
Worse: long-term steroid use depletes the barrier lipids it's made from. Each cycle leaves the barrier thinner than before. That's why you need more cream over time, and why stopping gets harder.
There's a name for this. Tachyphylaxis. Each steroid cycle makes your cortisol receptors less sensitive to the same dose. Your skin needs more to get the same result.
When you stop, those receptors rebound. Inflammation comes back harder than before. This is documented pharmacology.
Hajar et al. (2015), Journal of the American Academy of Dermatology — the National Eczema Association's own Task Force review — confirmed that topical steroid withdrawal is a real clinical consequence of long-term use.
One more thing. The Latin word sebum translates directly as tallow. Your skin's own oil and the primary ingredient in this product share the same two dominant fatty acids: oleic acid and palmitic acid.
These are two different interventions. One of them was never going to fix the other's problem.