Colorectal Cancer (CRC) is the third most leading cause of cancer related death worldwide and has a diverse clinical etiology. Mounting evidences has shown that CRC, in its rare yet lethal form as mucinous adenocarcinoma. Has led to poor prognosis and eventual complexity in the treatment. This subcategory of CRC characteristically secrete mucin hence, they are histologically identified based on the presence of mucin in CRC. In this context, the current article aims to provide a detailed overview and understanding of the underlying molecular mechanisms governing mucinous cancer onset and progression. We elaborate on the role of different pathways and molecular targets including microsatellite instability (MSI), chromosome instability (CIN) and CpG island methylator phenotype (CIMP), oncogenes such as KRAS, BRAF, p53 and p21 on mucinous CRC. The mucin genes, specifically MUC1, MUC4 and few other variants of the gel-secreted, transmembrane form of CRC play a vital role in the disease development. This makes the miRNA-mediated mucin regulations an exceptionally obliging aid in mucinous CRC understanding. The miRNAs discussed in context include miR-205, miR-373 and miR-124a to name a few. We further discuss the existing therapeutic strategies used to treat this variant of CRC. These diagnostic tools could help in the rapid identification and treatment of the disease.