Colorectal carcinoma is one of the most fatal cancers, but to date, the underlying mechanisms are not entirely understood. Recent epidemiological studies and clinical trials have begun to provide insights into the links between estrogens and colorectal carcinoma. The results obtained from established animal models indicated that abnormal high levels of estrogens promote the tumorigenesis of colitis-associated carcinoma. Estrogens regulate biological events mainly through two distinct receptors (Er alpha and Er beta). After combined with the receptor, estrogens translocate to nucleus and act as transcription factors to modulate several signaling pathways. Since organ destruction and parenchymal loss result in hormone inactivation disorder, patients with liver cirrhosis always have high levels of endogenous estrogens, which are the predominant causes of liver palm, spider angioma, gynecomastia, and testis atrophy. Meanwhile, several population-based studies confirmed that patients with liver cirrhosis face higher risks of colorectal carcinoma compared to general population. Although the influencing factors may be complicated, the high level of endogenous estrogens has been proposed as an important pathogen. Several studies, with the particular focus on menopause women, provided some contradictory results that estrogens may protect patients from cancers. However, the low levels of endogenous estrogens of menopause women, administration route, and the composition of drugs could lead to different conclusions. The exact effect of estrogens on the pathogenesis of colorectal carcinoma of a patient with liver cirrhosis is only just starting to be dissected.