As with mechanisms with intimate connections, liver damage is considered responsible for the alteration in the homeostatic system by inducing mechanisms such as transient thrombocytopenia, platelet inhibition, and prolonged clotting times, since the correlation between increased serum levels of enzymes of liver origin such as alanine aminotransferase (ALT) with coagulopathies during temperature elevations has been observed [27]. The gene discussed is GPT; the disease is Thrombocytopenia.