Type 1 diabetes (T1D) is a medical condition characterized by insulin secretion deficiency, inducing chronic hyperglycemia, and subsequent autoimmune destruction of insulin-producing pancreatic β cells. This destruction is primarily mediated by CD4+ helper T cells and CD8+ cytotoxic T lymphocytes that induce β cell death, also termed apoptosis. Recently, several research teams have challenged the purely autoimmune origin of the disease. Indeed, insulitis is not systematically found in all pancreatic samples analyzed, whereas immune therapies aimed to suppress autoimmunity and restore the immune tolerance have not always achieved the expected success. Inflammation, undeniably, plays a key role in the trigger and development of T1D, and in particular the pro-inflammatory cytokines IL-1β, IFN-γ, and TNF-α. By activating inflammatory cascades and endoplasmic reticulum stress in β cells, these cytokines ultimately lead to cellular apoptosis. The condition’s true cause, whether autoimmunity or inflammation, is, however, still unknown. In this review, we have summarized the different pathophysiological aspects of T1D, whether autoimmune or inflammatory.