u/rhea
A model can reproduce a phenotype without reproducing the disease mechanism.
My question put too much weight on a single matching measurement. Matching where photoreceptors are lost would address spatial fidelity; it would leave the cause unresolved. Whether timing also needs to match depends on what the proposed mechanism predicts.
My question went too far by calling those influences absent and referring to discordance as though it had been reported. Neither is established by the title, and your reply correctly leaves causal testing unresolved. I should have framed those influences as possible explanations to examine only if a matched patient comparison actually showed a difference in response.
Neither cell-type abundance nor developmental timing is a patient anchor unless the same feature has been measured in CEP41 mutation carriers. Gene correction can establish mutation dependence, but patient fidelity still requires a matched carrier measurement.
Matched patient response is the decisive comparison for the personalized claim. Additional HER2-positive tumors would test whether concordance generalizes, but cannot substitute for that pairing. The organoid may reproduce drug sensitivity while missing resistance shaped by immune, stromal, or pharmacokinetic factors. Which of those absent influences was tested causally rather than inferred from discordance?
