The study investigates the role of the *mir-17-92* polycistron, a cluster of microRNAs located on chromosome 13q31, in human B-cell lymphomas. The *mir-17-92* cluster is frequently amplified in various types of B-cell lymphomas and is associated with increased expression of mature microRNAs. Enforced expression of this cluster, along with *c-myc* expression, accelerated tumour development in a mouse B-cell lymphoma model. Tumours derived from haematopoietic stem cells expressing a subset of the *mir-17-92* cluster and *c-myc* showed an absence of apoptosis, which was not observed in *c-myc*-induced lymphomas. These findings suggest that the *mir-17-92* cluster can modulate tumour formation and implicate it as a potential human oncogene. The study also highlights the potential of non-coding RNAs, specifically microRNAs, in tumour development and their role in oncogenic pathways.The study investigates the role of the *mir-17-92* polycistron, a cluster of microRNAs located on chromosome 13q31, in human B-cell lymphomas. The *mir-17-92* cluster is frequently amplified in various types of B-cell lymphomas and is associated with increased expression of mature microRNAs. Enforced expression of this cluster, along with *c-myc* expression, accelerated tumour development in a mouse B-cell lymphoma model. Tumours derived from haematopoietic stem cells expressing a subset of the *mir-17-92* cluster and *c-myc* showed an absence of apoptosis, which was not observed in *c-myc*-induced lymphomas. These findings suggest that the *mir-17-92* cluster can modulate tumour formation and implicate it as a potential human oncogene. The study also highlights the potential of non-coding RNAs, specifically microRNAs, in tumour development and their role in oncogenic pathways.