The RAS-RAF-ERK pathway orchestrates a cascade of intracellular events that regulate cell growth, proliferation, and differentiation and its aberrant activation is a major driver of human cancer. The MRAS- SHOC2-PP1 (SHOC2 phosphatase) heterotrimeric complex plays an essential role in RAF-ERK pathway activation by dephosphorylating a specific phosphoserine site on RAF kinases. To investigate the function of SHOC2 in tissue homeostasis, we have generated Tamoxifen-inducible Cre mice that are homozygous for floxed SHOC2. To this end, we crossed SHOC2fl/fl conditional knockout (KO) mice with Rosa26-CreERT2 mice to generate SHOC2fl/fl KO Rosa26-CreERT2 mice, which carry an inducible ubiquitously expressed CreERT2 recombinase. The administration of tamoxifen results in highly effective recombination of more than 80% across all investigated tissues, excluding the brain. Serum biochemical assessment helps predict pathological processes in vital internal organs of the body, such as the liver, muscle, heart, pancreas, and kidney. To elucidate alterations in metabolism and organ functions resulting from systemic SHOC2 deletion, blood was collected from wildtype and SHOC2 knockout mice via cardiac puncture at morbidity, and serum biochemical parameters were analysed. The blood test for the biochemistry profile included a series of biomarkers for liver and kidney functions, lipid levels, electrolytes, as well as additional metabolic markers such as glucose, fructose, total protein, and albumin. Most of the serum chemistry parameters were unaffected suggesting SHOC2 inactivation does not cause major and/or clear alterations in liver or kidney function. However, albumin, total cholesterol, high-density lipoprotein, glucose, fructose and alkaline phosphatase levels were significantly decreased in SHOC2 KO mice compared to wild type controls. While the significance of these changes is unclear, they are consistent with the weight loss that was observed in the SHOC2 KO mice at the time of analysis and thus may be the reflection of weight loss like consequence rather than the cause.