This review discusses the role of microRNAs (miRNAs) in cell proliferation, cell death, and tumorigenesis. MiRNAs are small non-coding RNAs that negatively regulate target mRNAs, playing crucial roles in various cellular functions. Abnormal miRNA expression is common in human malignancies, and this review highlights how miRNAs influence tumorigenesis by acting as both oncogenes and tumor suppressors. The biogenesis of miRNAs involves the transcription of primary miRNAs (pri-miRNAs) by RNA polymerase II, followed by processing by Drosha and Dicer to form mature miRNAs. These mature miRNAs are then incorporated into the RNA-induced silencing complex (RISC), where they guide the silencing of target mRNAs. Early clues that miRNAs regulate cancer-relevant pathways came from genetic screens in *Caenorhabditis elegans* and *Drosophila*. For example, the lin-4 miRNA controls developmental timing, and its loss leads to abnormal cell differentiation. In *Drosophila*, overexpression of the Bantam miRNA promotes cell proliferation and prevents apoptosis, while miR-14 suppresses cell death. In cancer, miRNA dysregulation is a frequent occurrence. For instance, the *mir-17* cluster, located on chromosome 1q31, is frequently amplified in lymphomas and solid tumors. Overexpression of this cluster accelerates cell proliferation and suppresses apoptosis. Similarly, miR-21 is overexpressed in glioblastoma and breast cancer, promoting cell proliferation. Antiproliferative and proapoptotic miRNAs, such as let-7, miR-15a, and miR-16-1, function as tumor suppressors. Let-7 targets RAS genes, which are potent oncogenes, and its loss is associated with shorter survival in lung cancer patients. MiR-15a and miR-16-1 target BCL2, a potent inhibitor of cell death, and their loss contributes to elevated Bcl2 expression and pathologic cell survival in chronic lymphocytic leukemia. The review also discusses the role of miRNAs in cell cycle progression and stem cell maintenance, suggesting that miRNAs may play a role in stem cell maintenance and that their functions can vary depending on the tissue type. In conclusion, miRNAs are essential in various physiological processes and their dysregulation can lead to tumorigenesis. Further research is needed to identify and validate critical targets of miRNAs in cancer, and to understand the tissue-specific functions of miRNAs.This review discusses the role of microRNAs (miRNAs) in cell proliferation, cell death, and tumorigenesis. MiRNAs are small non-coding RNAs that negatively regulate target mRNAs, playing crucial roles in various cellular functions. Abnormal miRNA expression is common in human malignancies, and this review highlights how miRNAs influence tumorigenesis by acting as both oncogenes and tumor suppressors. The biogenesis of miRNAs involves the transcription of primary miRNAs (pri-miRNAs) by RNA polymerase II, followed by processing by Drosha and Dicer to form mature miRNAs. These mature miRNAs are then incorporated into the RNA-induced silencing complex (RISC), where they guide the silencing of target mRNAs. Early clues that miRNAs regulate cancer-relevant pathways came from genetic screens in *Caenorhabditis elegans* and *Drosophila*. For example, the lin-4 miRNA controls developmental timing, and its loss leads to abnormal cell differentiation. In *Drosophila*, overexpression of the Bantam miRNA promotes cell proliferation and prevents apoptosis, while miR-14 suppresses cell death. In cancer, miRNA dysregulation is a frequent occurrence. For instance, the *mir-17* cluster, located on chromosome 1q31, is frequently amplified in lymphomas and solid tumors. Overexpression of this cluster accelerates cell proliferation and suppresses apoptosis. Similarly, miR-21 is overexpressed in glioblastoma and breast cancer, promoting cell proliferation. Antiproliferative and proapoptotic miRNAs, such as let-7, miR-15a, and miR-16-1, function as tumor suppressors. Let-7 targets RAS genes, which are potent oncogenes, and its loss is associated with shorter survival in lung cancer patients. MiR-15a and miR-16-1 target BCL2, a potent inhibitor of cell death, and their loss contributes to elevated Bcl2 expression and pathologic cell survival in chronic lymphocytic leukemia. The review also discusses the role of miRNAs in cell cycle progression and stem cell maintenance, suggesting that miRNAs may play a role in stem cell maintenance and that their functions can vary depending on the tissue type. In conclusion, miRNAs are essential in various physiological processes and their dysregulation can lead to tumorigenesis. Further research is needed to identify and validate critical targets of miRNAs in cancer, and to understand the tissue-specific functions of miRNAs.