NIT1 (nitrilase 1) is a metabolite repair enzyme that catalyzes hydrolysis of deaminated glutathione (dGSH), a harmful byproduct generated by transaminases during primary metabolism 1. This repair function prevents accumulation of non-functional dGSH and is physiologically significant, with NIT1 deficiency linked to neurological disorders 2. Beyond its enzymatic role, NIT1 functions as a tumor suppressor through multiple mechanisms. It directly interacts with the tumor suppressor FHIT, forming a tetrameric complex 3, and suppresses colorectal cancer proliferation by activating TGFβ1-Smad2/3 signaling pathways 4. NIT1 loss of expression promotes cell growth and resistance to DNA damage stress while increasing NMBA-induced tumor incidence. In cancer cells, NIT1 enhances apoptotic responsiveness additively with FHIT's tumor suppressor activity 5. NIT1 also acts as a negative regulator of primary T cells. The protein localizes to the mitochondrion, nucleus, and cytoplasm, reflecting its dual roles in metabolic repair and tumor suppression. These findings suggest NIT1 represents a convergence point between fundamental metabolic homeostasis and cancer prevention.