In 1927 Guido Fanconi described a hereditary condition presenting panmyelopathy accompanied by short stature and hyperpigmentation, now better known as Fanconi anemia (FA). With this discovery the genetic and molecular basis underlying FA has emerged as a field of great interest. FA signaling is crucial in the DNA damage response (DDR) to mediate the repair of damaged DNA. This has attracted a diverse range of investigators, especially those interested in aging and cancer. However, recent evidence suggests FA signaling also regulates functions outside the DDR, with implications for many other frontiers of research. We discuss here the characteristics of FA functions and expand upon current perspectives regarding the genetics of FA, indicating that FA plays a role in a myriad of molecular and cellular processes.

1927年，圭多·范科尼（Guido Fanconi）描述了一种遗传性疾病，表现为伴有身材矮小和色素沉着过多的潘氏骨髓病，现在被称为范科尼贫血（FA）。有了这一发现，FA的遗传和分子基础已经成为人们非常感兴趣的领域。FA信号在DNA损伤反应（DDR）介导受损DNA修复中至关重要。这吸引了各种各样的研究者，尤其是那些对衰老和癌症感兴趣的研究者。但是，最近的证据表明，FA信号传导还调节DDR以外的功能，这对许多其他研究领域都有影响。我们在这里讨论FA功能的特征，并在有关FA遗传学的当前观点上进行扩展，这表明FA在无数的分子和细胞过程中都发挥着作用。