Mimitin, a small mitochondrial protein, whose transcription is directly stimulated by c-Myc, is highly expressed in 80% of esophageal squamous cell carcinomas (ESCC). Suppression of Mimitin expression by RNA interference had no effect in cancerous cell lines such as human cervical carcinoma or hepatocarcinoma cell lines, but caused a decrease in cell proliferation in human glioblastoma, embryonic lung fibroblastic cells, and ESCC, suggesting Mimitin may play a special role in these types of cells. Mimitin expression is also regulated by MAPK kinases and IL-1, but not through the NF-kappaB-related pathway. It will interact with the microtubular protein MAP1S and can affect the activities of caspase-3 and -7 in cells stimulated to develop apoptosis. Other experiments suggest that Mimitin also acts as a molecular chaperone for the assembly of the mitochondrial complex I.