Ethylene, often referred as “death hormone” for its role in plant abscission, senescence, and fruit ripening, is a simple olefin gas and the first gaseous hormone discovered in plants. It also regulates seed germination, root and shoot growth, flower development, fruit ripening, and responses to biotic and abiotic stresses. Ethylene biosynthesis initiates with methionine converting enzymatically to S-adenosyl-L-methionine (SAM), then to 1-aminocyclopropane-1-carboxylic acid (ACC) by ACC synthase (ACS), and finally to ethylene via ACC oxidase (ACO). Its production is regulated at transcriptional, post-transcriptional, and post-translational levels. Ethylene sensing depends on receptors such as ETR1 and ERS1, located on the endoplasmic reticulum. When ethylene binds these receptors, CTR1 becomes inactive, allowing EIN2 to relay signal to transcription factors EIN3/EIL1 and ERFs. As this pathway can interact with auxin, jasmonic acid, salicylic acid, abscisic acid, and gibberellins, it coordinates plant growth and stress management. Ethylene affects root system architecture, particularly under varying phosphate availability, modifying root hair development to enhance nutrient uptake. It also shapes plant immunity by modifying defense response against biotic and abiotic challenges. Advances such as ethylene-sensitive fluorescent reporters, genomic and proteomic tools, and computational models have clarified many aspects of ethylene signaling. However, key questions remain, including the precise activation mechanism of ethylene receptors, details of hormonal crosstalk, and post-translational modifications.