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Metabolic tumor suppression runs through Stk11, the mouse ortholog of human STK11 (LKB1), a serine and threonine kinase that must complex with the pseudokinase STRADA and the scaffold CAB39 to adopt an active conformation, whereupon it phosphorylates the activation loop threonine of AMPK alpha subunits and of twelve related kinases including the SIK, NUAK, MARK, and BRSK families, linking energy stress to mTORC1 restraint, epithelial polarity, and CRTC-dependent transcription. Germline heterozygous inactivation causes Peutz-Jeghers syndrome with hamartomatous polyposis, and somatic biallelic loss co-occurs with KRAS mutation in lung adenocarcinoma, producing immunologically cold, STING-silenced tumors whose SIK dependence and serine metabolism define distinct vulnerabilities. Germline nulls die in midgestation from vascular and placental defects, so conditional nulls combined with Kras LSL-G12D and viral Cre delivery are the workhorse design, while kinase-dead or Peutz-Jeghers missense knockins separate catalytic from scaffolding function. Choose allele class by endpoint: polyposis, tumor immunophenotype, or metabolic inhibitor response.

Stk11 conditional knockout mice carry a floxed allele so you delete function only where Cre is active. The germline allele stays intact until you cross to a tissue specific Cre. Labs reach for this design when a global knockout is lethal, when they need adult onset loss, or when regional redundancy hides a whole body phenotype. For liver work, plan Cre specificity, reporter crosses, and baseline phenotyping before you scale.