The study of normal and pathological states of the gene network regulating cholesterol biosynthesis in the cell is a topical problem. Impairments of this system play a key role in the development of hypercholesterolemia and atherosclerosis of humans and various animals. Knowledge of the behavior of this system under various conditions is necessary to develop optimal strategies for correcting various pathologies while taking into account the genotype-specific distinctions of individuals and the targets for pharmacological regulation. The model simulating cholesterol biosynthesis in the cell and its exchange with blood plasma cholesterol developed earlier using a generalized chemical kinetic approach was used for the analysis of a mutational portrait of this system. The sensitivity of the stationary content of free cholesterol to mutational changes in the rates of molecular processes running within the gene network was analyzed. The resilience of the free cholesterol concentration to a wide range of mutations in the gene network was demonstrated. In addition, it was shown that the mutations hitting regulatory processes changed the stationary content of free cholesterol to the largest degree.