## 1 Introduction  
Colorectal cancer is second in incidence in women after breast cancer, followed in third and fourth place by lung and cervix cancers, respectively. In men, lung cancer is the highest in incidence, with prostate cancer being the second, followed in third place by colorectal cancer. Despite the important advances in its treatment, colorectal cancer remains the second cause of death from cancer considering the general population, with an estimated mortality in both sexes worldwide in 2018 of 880,792 deaths [1,2]. In the United States, colorectal cancer is the third most common cancer diagnosed in both sexes, and The American Cancer Society estimates 104,610 new cases of colorectal cancer will occur in 2020 [3]. In Spain, the colorectal cancer was the cancer most frequently diagnosed in both sexes in 2019 (with 44,937 new cases), the second in men after prostate cancer, and the second in women after breast cancer [4]. There seems to be a process with multiple stages of evolution from the normal colonic mucosa to a potentially fatal carcinoma. Cells, which must have a certain genetic predisposition or suffer a series of genotoxic phenomena, are induced to proliferate, thus passing through a series of stages until they end up doing so in a completely uncontrolled manner. One of the proto-oncogenes that can be altered in this process is KRAS, which is involved in the pathway of transduction of growth signals and cell differentiation. It is estimated that 65% of sporadic colorectal carcinomas present activation by point mutations in a gene of the RAS family (mainly KRAS) [5]. The RAS gene is now part of the criteria of the new TNM classification of malignant tumours as a prognostic and predictive factor, since patients with early stage colorectal cancer (I and II) have a lower survival rate when related to the KRAS mutation. In patients with metastatic colorectal cancer, the median overall survival without treatment is approximately 6 months. With the use of current therapies, survival can be prolonged to a median of 30 months, with a response rate for some therapies of 50% [6]. The introduction of targeted therapies resulted in an increase in progression-free survival and also in overall survival in patients with metastatic colorectal cancer. Therefore, in addition to combined chemotherapy regimens, there are currently a series of agents that act against certain specific targets important in the pathological process of CRC (colorectal cancer). These therapies are monoclonal antibodies against EGFR, monoclonal antibodies against VEGF-A, and also fusion proteins against multiple molecules and growth factors. For the use of this targeted therapy, the existence of mutations in KRAS and NRAS must be previously verified. If these mutations are present, the tumour cell presents an activation of multiple signalling pathways that render useless the targeted treatment against those genes [7]. Therefore, it has been described that mutations in the KRAS proto-oncogene cause a poor response to anti-EGFR treatment in cases of metastatic colorectal cancer. The presence or absence of this mutation must be confirmed, because patients with colorectal cancer who present native KRAS can benefit from targeted therapy with anti-EGFR [8,9]. Radiological images contain information about the underlying pathophysiology that can be extracted through a quantitative analysis of the texture of the image [10,11]. With radiomics, analysing the relationship between the intensity/density of the pixels that make up the texture of the tumour image, we could obtain an identifative pattern of an underlying pathophysiological alteration, as has already been demonstrated in other tumours using other radiological techniques [12, 13, 14, 15, 16, 17]. This information is different from that provided by laboratory tests and other pathological or genomic analysis.