While drift-related risk cannot be entirely avoided, we tried to reduce it by: (i) running independent families within HAB, NAB and LAB lines [16]; (ii) replicating key findings of c-Fos expression in both mice and rats, using similar inbreeding protocols (this study and [13]); and (iii) showing that, in a pharmacological validation approach, paroxetine treatment attenuated both c-Fos expression and depression-like behaviour [11], further confirming an association between neuronal excitability and the behavioral phenotype beyond genetic drift. The gene discussed is FOS; the disease is depressive symptom measurement.