Stevens-Johnson syndrome and toxic epidermal necrolysis are both severe hypersensitivity responses caused by drugs. The mechanisms at work are not completely understood. In this paper, researchers have discussed recent findings on both mechanistic and genetic variables connected to these disorders and offer future ways to unravel their complexities. Several variations in the human leukocyte antigen area have been related to these responses, according to genome-wide association studies. These are very reliant on the demographic investigated as well as the substance used to activate them. Also important is the patient’s T-cell receptor repertoire. Interactions between Fas-Fas and its ligands, as well as perforin and granulysin, have been identified as key participants. Furthermore, a high-throughput gene expression research found a number of genes whose expression increases in patients during the acute phase of these responses. This study evaluated current high-throughput research on these disorders and proposes methods for combined and reanalyzed data usage integrated systems biology tools. It also proposed future areas of inquiry that might shed further light on their underlying processes by utilizing cutting-edge technology.