Experiments show that transferring a cancer cell's dysfunctional mitochondria—but not its nucleus—into a healthy cell is what induces cancer. This disruptive finding supports the view of cancer as a metabolic disease that can be targeted by starving its mitochondria of fuels like glucose.

Dr. Levin's lab uses voltage-sensitive dyes to visualize bioelectric patterns that act as functional memories of a body's target anatomy. These patterns are not just activity; they are decodable, rewritable blueprints that guide regeneration and development, determining the final anatomical outcome.

Dr. Levin argues that neuroscience's true subject is the architectural principles of "cognitive glue"—how simple components combine to form larger-scale minds. He believes this process is not unique to neurons and that the field's current focus is too narrow, missing applications in cellular biology, AI, and beyond.

Dr. Levin reframes the placebo effect as a primary feature of biology to be studied, not an experimental nuisance. He equates it to voluntary motion, where abstract thoughts directly control cellular chemistry. This suggests a powerful, built-in mechanism for top-down cognitive control over the body's physiology.

Instead of targeting individual gene mutations in diseases like ALS, condensate science focuses on shared cellular structures where genetic risks converge. This approach creates a broader therapeutic target, potentially treating more patients with diverse genetic profiles.

The efficacy of some established drugs, like the chemotherapy oxaliplatin, may be due to an unknown mechanism: they partition into and disrupt cellular condensates. This reframes our understanding of drug action and could explain why certain drugs are more effective in some cancers than others.

Dr. Levin proposes that aging may occur because the body's goal-seeking cellular system achieves its primary goal (building a body) and then degrades due to a lack of new directives. This contrasts with damage-based theories and is supported by immortal planaria, which constantly challenge themselves by regenerating.

Cellular senescence is a biological process that permanently halts cell division. Contrary to being just a sign of aging, its primary function is to prevent damaged cells from becoming cancerous. It's a protective measure that stops unchecked proliferation when a cell cannot repair its own damage or undergo programmed cell death.

Dr. Michael Levin argues that DNA specifies cellular hardware, but bioelectric patterns act as reprogrammable software that stores anatomical memories. This software can be rewritten to produce radical changes, like two-headed worms, without altering the genetic code, challenging the DNA-centric view of biology.