Tumours are constituted of a heterogeneous mixture of cells, which are subject to selective pressures leading to the evolution of cell populations over time. By applying a variety of methods to multiomic data, we model the effect of tumour evolutionary processes in terms of the multimodal molecular signature that they leave. This signature is composed of a combination of different types of aberration, including copy number, point mutation and methylation changes. Using examples from a range of tumour types including prostate, oesophageal, breast and haematopoietic cancers, I will describe the findings that may be obtained from 2 different types of study: deep studies involving multiomic, multiple-sample data from a small number (10s) of tumours and studies involving relatively shallow analysis of single samples from a large number (1000s) of tumours.