Oliver's mTOR Atlas Evidence Platform
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mTOR Academy · Qualifying Exam

Think you can reason like an mTOR researcher?

Ten hard questions, about five minutes, no account. You don't need to know everything. You need to know what the evidence actually allows you to claim.

Can you make Postdoc? Nine of ten with good calibration makes Postdoc. You are placed by how many you get right and by how well your confidence matches your accuracy.

What the exam asks

The exam needs JavaScript to score and place you. Here are three of the kinds of question it draws from, with answers.

Rapamycin raises AKT Ser473 phosphorylation in a cancer cell line. Which experiment best separates released S6K1–IRS-1 feedback from a direct off-target action of the drug on AKT?
  1. Repeat at ten times the dose and check that the rise gets larger
  2. Remove the upstream route (knock down IRS-1, or block IGF-1R/PI3K) and repeat: if released feedback is the cause, the rise should largely disappear
  3. Blot for phospho-S6 to confirm that mTORC1 was inhibited
  4. Repeat the experiment in a second cell line

Answer: B. The feedback hypothesis names a route: S6K1 normally restrains IRS-1, so the AKT rise should need IRS-1 and the receptor above it. Cutting that route tests the hypothesis directly; a drug acting on AKT itself would survive it. Phospho-S6 only shows the drug reached mTORC1, and a higher dose or another cell line changes the size of the effect without telling the two explanations apart. ORE2006 blocked the IGF-1 receptor for exactly this reason.

Which limitation is the one this study states about itself?

mTOR regulates memory CD8 T-cell differentiation (2009, Mouse)
mTOR is a key regulator of memory CD8 T-cell differentiation; rapamycin enhances memory responses.
Sample: not stated

  1. No lifespan or healthspan endpoint. Side-effect endpoints only; benefit retention is inferred, not tested.
  2. Inference from a single exceptional responder; basis of mTOR-inhibitor sensitivity incompletely understood; short drug exposure in some.
  3. FDA changed the primary endpoint between phase 2b and phase 3 (symptom-based vs lab-confirmed), complicating comparison; positive biomarker did not translate to…
  4. mTOR knockdown does not completely mimic rapamycin treatment.

Answer: D. Its own limitation, as recorded in the Atlas: mTOR knockdown does not completely mimic rapamycin treatment.

How settled is this, as the field stands?

Unphosphorylated 4E-BP1 clamps onto eIF4E and stops it assembling the cap-binding complex. mTORC1 phosphorylates 4E-BP1 to release that grip - so the brake on translation is released, not the accelerator pressed.

  1. Established
  2. Emerging
  3. Contested
  4. Open — no answer either way

Answer: A. Curated in the Atlas as consensus established, mechanistic evidence high, human relevance plausible. Scope: Biochemical and cell-culture evidence (in vitro assays, mammalian and mouse cells, plus one review). It establishes the binding switch itself. It does not measure how much translation changes in a…

How placement works

9 or more right: Postdoc if your Brier score is 0.16 or lower. 7 or more right: Graduate if your Brier score is 0.2 or lower. 5 or more right: Rotation Student. 3 or more right: Student.

Principal Investigator is not examined. It is earned in the Practice Arena, where the rank-up boards also check calibration. Where you disagree with how the Atlas labels a pathway step, say so under the answer: a curator checks every report against the studies behind the label.

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