In LKB1-deficient non-small cell lung cancer (NSCLC) models, AMPK inactivation derepresses CPS1, whose silencing induces nucleotide pool imbalance (reduced pyrimidine/purine ratio), S-phase arrest, and DNA damage, mechanisms hypothesized to operate in PCa, where ammonium metabolism inhibitors (e.g., targeting glutaminase) combined with autophagy modulators (e.g., ULK1 activators) could exploit metabolic vulnerabilities targeting tumor cells (200). This evidence concerns the gene CPS1 and non-small cell lung carcinoma.