Moreover, using a genetically engineered mouse model of lung adenocarcinoma development driven by KrasG12D (the KrasLSL-G12D mouse) and several biochemical and genetic approaches, including in vivo xenotransplantation studies, researchers demonstrated that a loss of function of PLCγ1 leads to the increased expression of glycolytic genes, increased tumor growth, and decreased survival. Here, PLCG1 is linked to neoplasm.