Septic shock is provoked by hyper-activation of the pro-inflammatory response after infection and the patient requires anti-inflammatory treatment. However, the immune system develops a compensatory mechanism where the resulting feedback leads to an anti-inflammatory response after the initial state, which is referred to as immunodeficiency. Therefore, the initial therapeutic treatment with anti-inflammatory intervention has failed for almost 20 years and it has been changed in the last 10 years based on modulation of the inflammatory response. Using in silico methods, it is possible to develop a new approach based on physiopathology for treating septic shock. According to our new mathematical model, we can consider the dysfunctional immune system in a patient with septic shock and modify two parameters at different times to determine a possible treatment, and bearing out the single nucleoid polymorphism (SNP) may predominate the further deterioration of sepsis. The result represents the initial anti-inflammatory treatment with interleukin-10 activation and an increased risk of mortality over time for the septic shock patient, excluding the early stages. However, a hypothetical treatment based on interleukin-10 inhibition can change the patient's immune stage and provide a new therapy according to our results, and show that the frequency of pro-inflammatory related gene SNP can be the possibility of increase sepsis risk. In conclusion, our proposed in silico method can explore therapeutic strategies and predict their associated efficacy and important factors, with the ultimate objective of improving treatments to reduce mortality.