Dengue fever (DF) is a significant public health problem in the African continent. The primary prevention strategy against the disease is vaccination and entomological control of vectors; however, implementing such a strategy in several countries in the continent is far below what is necessary to control the disease. The Coronavirus disease (COVID‐19) pandemic further aggravated this situation and negatively impacted these measures, mainly the coverage of vaccination campaigns, due to restrictive measures to control the disease. Therefore, the most significant risk is that the incidence of DF in the continent will increase even more in the coming years, as a reflection of the negative impact of the pandemic on the control of the disease. To prevent another public health crisis, immediate and multidisciplinary approaches are required to address the epidemiological control of DF in African countries.

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Resistance to tyrosine kinase inhibitors (TKIs) of the epidermal growth factor receptor (EGFR) in advanced mutant Non-Small Cell Lung Cancer (NSCLC) constitutes a therapeutic challenge. This review intends to summarize the existing knowledge about the mechanisms of resistance to TKIs in the context of EGFR mutant NSCLC and discuss its clinical and therapeutic implications. EGFR-dependent and independent molecular pathways have the potential to overcome or circumvent the activity of EGFR-targeted agents including the third-generation TKI, osimertinib, negatively impacting clinical outcomes. CNS metastases occur frequently in patients on EGFR-TKIs, due to the inability of first and second-generation agents to overcome both the BBB and the acquired resistance of cancer cells in the CNS. Newer-generation TKIs, TKIs targeting EGFR-independent resistance mechanisms, bispecific antibodies and antibody-drug conjugates or combinations of TKIs with other TKIs or chemotherapy, immunotherapy and Anti–Vascular Endothelial Growth Factors (anti-VEGFs) are currently in use or under investigation in EGFR mutant NSCLC. Liquid biopsies detecting mutant cell-free DNA (cfDNA) provide a window of opportunity to attack mutant clones before they become clinically apparent. Overall, EGFR TKIs-resistant NSCLC constitutes a multifaceted therapeutic challenge. Mapping its underlying mutational landscape, accelerating the detection of resistance mechanisms and diversifying treatment strategies are essential for the management of the disease.

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