Despite the changing demography and patient profile, the etiology of common fungal infections remains largely unchanged. Aspergillus, Candida, dimorphic fungi like Histoplasma capsulatum, Blastomyces spp., Coccidioides spp., Mucormycetes, Cryptococcus species, and Pneumocystis jirovecii cause the majority of fungal infections. Antifungal resistance, intrinsic or acquired, is developing at an alarming pace and has grave consequences. Cryptococcus is intrinsically resistant to echinocandins while Aspergillus fumigatus is acquiring resistance to the azole group. Immunosuppression in hosts due to HIV, solid organ transplant, human stem cell transplant, and diabetes plays a role in development of resistance. Other factors that play a role in building resistance are: delay in the initiation of a targeted therapy, inaccurate doses, poor absorption of the therapeutical agent to the site of infection, insufficient knowledge of pharmacokinetics, interactions of antifungals with other therapeutical agents, and lack of fungicidal agents. While the world faces the increasing problem of antifungal resistance, new, more dangerous fungal species are emerging. Candida auris is one such recently emerged fungal pathogen. It poses a serious global threat to public health and can spread efficiently in healthcare facilities, causing prolonged healthcare-associated outbreaks. This pathogen has a unique ability to colonize the human skin and mucosa, persisting on surfaces of hospital and nursing home environments, including bed rails and medical equipment, causing difficult-to-eradicate outbreaks. There is an urgent need for more research to understand the epidemiology, diagnosis, and management of azole-resistant Aspergillus fumigatus. Understanding of the molecular mechanisms of resistance is critical to developing effective treatment strategies and preventing the spread of resistant strains.