By normalizing the inflammatory response, as evidenced by normalization of IL-10, and activating the neuroprotective heat shock response without pharmacologic agents or infectious stimuli, CBIT2 provides a molecularly grounded and clinically actionable strategy for the restoration of motor neurons in ALS, a disease historically defined by relentless progression, therapeutic failure, irreversibility, and fatal outcomes. This evidence concerns the gene IL10 and amyotrophic lateral sclerosis.