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Following presynaptic dopamine and glutamate co-release by such psychostimulants, ΔFos B functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.

Fos B and its truncated splice variants, ΔFos B and further truncated Δ2ΔFos B, are all involved in osteosclerosis, although Δ2ΔFos B lacks a known transactivation domain, in turn preventing it from affecting transcription through the AP-1 complex.This change can be identified rather quickly, and may be sustained weeks after the last dose of the drug.Transgenic mice exhibiting inducible expression of ΔFos B primarily in the nucleus accumbens and dorsal striatum exhibit sensitized behavioural responses to cocaine.ΔFos B overexpression (i.e., an abnormally and excessively high level of ΔFos B expression which produces a pronounced gene-related phenotype) triggers the development of addiction-related neuroplasticity throughout the reward system.ΔFos B differs from the full length Fos B and further truncated Δ2ΔFos B in its capacity to produce these effects, as only accumbal ΔFos B overexpression is associated with pathological responses to drugs.

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