Our evolutionary biology doesn't "care" if we get cancer. Just that we have healthy children and can rear them for one or two generations. That was a (locally) optimal algorithm.

We have plenty of in-built checks and protections in our molecular biology, and they are sufficient to expand the species.

That HN comment is partly correct, but it oversimplifies and mixes some truths with speculation. Let’s break it down:

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### Points that are basically correct:

* *Cancer and immune systems:* The immune system does play a crucial role in suppressing tumors (immune surveillance). As it weakens with age (immunosenescence), cancer risk rises in humans. So the link between cancer and immune system strength is real.

* *Species differences:* Some animals are notably resistant to cancer. For example, *naked mole-rats* and *elephants* have special mechanisms that reduce cancer incidence. Elephants, for instance, have extra copies of the *p53 tumor suppressor gene*, and naked mole-rats have unique extracellular matrix components (high molecular weight hyaluronan).

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### Points that are misleading or wrong:

* *“Bats basically never get cancer”:* Not true. Bats do get cancer, but at apparently lower rates than expected given their size and lifespan. Research suggests their DNA repair mechanisms, dampened inflammation, and immune adaptations for long flight and viral tolerance may contribute to lower incidence. But “never” is an exaggeration.

* *“Mice die of cancer because their immune systems are really bad”:* Oversimplified. Mice in labs are inbred, live in artificial conditions, and are predisposed to certain cancers. But the main reason is *life history strategy*: mice are small, reproduce fast, and evolutionary pressure favors rapid reproduction over long-term somatic maintenance. Their “bad immune system” isn’t a flaw so much as an evolutionary tradeoff.

* *“Cancer in mammals is only about failing immune systems, not raw age”:* Not quite. Cancer incidence is influenced by *multiple factors*:

  * Number of cell divisions (bigger, longer-lived animals should face more cancer risk, but many evolved defenses → *Peto’s paradox*).
  * DNA repair mechanisms.
  * Immune function.
  * Metabolism and oxidative stress.
  * Random mutations.
    Age is still a huge risk factor in humans because mutations accumulate and repair processes decline, not only because the immune system weakens.

### So, overall:

* The commenter is right that *immune competence matters a lot* for cancer resistance. * They are wrong to frame it as “bats = immune gods, mice = immune failures.” It’s really about *evolutionary tradeoffs and multiple defense layers*. * Cancer risk isn’t just immune-system-dependent; it’s also tied to mutation accumulation, DNA repair fidelity, tumor suppressor genes, and life history strategies.

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Do you want me to rewrite that HN comment in a way that would be factually solid (like how an actual researcher might put it)?

Which effect size do you find lacking?

I meant where do you get enough stem cells to make the procedure widely available to the developed world? Stem cells are kinda scarce, as far as I know, so it may gate such a thing.