The rapid progress of Internet technology has led to a strong increase in the use of online social networks for disseminating information on the Internet. In this scenario, it is crucial to establish approaches that can effectively reduce the diffusion of false information (fake news) that can potentially cause harm to society. A defensive approach, based on integer-order differential equations, has been recently developed to analyze the effects of verification and blocking of users for containing the spread of fake news. Starting from it, we introduce a novel fractional model providing a more accurate, powerful, and realistic representation of the transmission of fake news messages. The model aims to predict the spread of such messages, by better considering the effect of the system's status evolution over time. The use of fractional differential equations to schematize the propagation of fake news results in incorporating a greater amount of memory information and better considering hereditary properties of the system of interest, also capturing its hidden nonlinear dynamics, mainly related to fractality and multiscale nature.

K-Ras activating mutations are significantly associated with tumor progression and aggressive metastatic behavior in various human cancers including pancreatic cancer. So far, despite a large number of concerted efforts, targeting of mutant-type K-Ras has not been successful. In this regard, we aimed to target this oncogene by a combinational approach consisting of small peptide and small molecule inhibitors. Based on a comprehensive analysis of structural and physicochemical properties of predominantly K-Ras mutants, an anti-cancer peptide library and a small molecule library were screened to simultaneously target oncogenic mutations and functional domains of mutant-type K-Ras located in the P-loop, switch I, and switch II regions. The selected peptide and small molecule showed notable binding affinities to their corresponding binding sites, and hindered the growth of tumor cells carrying K-RasG12D and K-RasG12C mutations. Of note, the expression of K-Ras downstream genes (i.e., CTNNB1, CCND1) was diminished in the treated Kras-positive cells. In conclusion, our combinational platform signifies a new potential for blockade of oncogenic K-Ras and thereby prevention of tumor progression and metastasis. However, further validations are still required regarding the in vitro and in vivo efficacy and safety of this approach.