Summary Results from comparative and ecological wood anatomy combined with a number of experimental studies on plant hydraulics have led to a pervasive and longstanding assumption that wider-diameter vessels are more vulnerable to drought-induced embolism than narrower vessels. Although we agree that wider vessels tend to be more vulnerable than narrower vessels within stems and within roots across most species, our current understanding of the diameter-vulnerability link does not offer a mechanistic explanation for why increased vessel diameter should consistently lead to greater vulnerability or vice versa. Causes of drought-induced embolism formation and spread likely operate at the nano-level, especially at gas-liquid-surfactant interfaces inside intervessel pit membranes. We evaluate here new perspectives on drought-induced embolism and its key anatomical and physico-chemical drivers, of which vessel diameter is one of the parameters involved, although its linkage to embolism vulnerability is likely indirect. As such, the diameter-vulnerability link does not imply that species with on average wider vessels are consistently more susceptible to drought-induced embolism compared to species with narrower vessels. Scientific priorities for future progress should focus on more accurate predictions of how water transport in plants is affected by drought, which requires a better mechanistic understanding of xylem network topology and biophysical processes at the nano-scale level in individual vessels that determine embolism formation and spread.