良性肿瘤的分子发病机制认识可能带来关键信息，以澄清肿瘤发生过程，并最终加深对癌变等过程的了解。良性新生物的定义不总是清晰，本文讨论了围绕此概念的问题。良性新生物与恶性肿瘤共享除转移潜力外的所有癌症标志。最近，下一代测序提供了解开良性新生物基因基础的前所未有的机会。迄今为止，我们已经了解到良性新生物确实特征是存在基因突变，包括基因重排。在晚期癌症中，驱动突变是这些突变会带来生长优势，并在癌症进化过程中积极选择的突变。本文将在癌症预防的背景下讨论这一概念，包括前体病变和良性新生物。在考虑早期检测和癌症预防时，驱动突变不仅应具有优势（即带来存活优势），而且应具有易感性（即促进癌症表型）。通过包括恶性新生物的良性对应物进行肿瘤生物学研究，可以评估给定突变带来的风险，并区分优劣突变，进一步完善驱动突变的概念。因此，应该鼓励良性新生物的研究，因为它提供了关于肿瘤发生的宝贵信息，对于理解从发生到恶化的进程是至关重要的。版权所有© 2022 Elsevier B.V.。保留所有权利。

The understanding of the molecular pathogenesis of benign tumors may bring essential information to clarify the process of tumorigenesis, and ultimately improve the understanding of events such as malignant transformation. The definition of benign neoplasia is not always straightforward and herein the issues surrounding this concept are discussed. Benign neoplasms share all cancer hallmarks with malignancies, except for metastatic potential. Recently, next-generation sequencing has provided unprecedented opportunities to unravel the genetic basis of benign neoplasms and, so far, we have learned that benign neoplasms are indeed characterized by the presence of genetic mutations, including genes rearrangements. Driver mutations in advanced cancer are those that confer growth advantage, and which have been positively selected during cancer evolution. Herein, some discussion will be brought about this concept in the context of cancer prevention, involving precursor lesions and benign neoplasms. When considering early detection and cancer prevention, a driver mutation should not only be advantageous (i.e., confer survival advantage), but predisposing (i.e., promoting a cancer phenotype). By including the benign counterparts of malignant neoplasms in tumor biology studies, it is possible to evaluate the risk posed by a given mutation and to differentiate advantageous from predisposing mutations, further refining the concept of driver mutations. Therefore, the study of benign neoplasms should be encouraged because it provides valuable information on tumorigenesis central for understanding the progression from initiation to malignant transformation.Copyright © 2022 Elsevier B.V. All rights reserved.