This signaling pathway elicited by ponatinib resembles that of ECs exposed to atheroprone stimuli, such as disturbed flow, reactive oxygen species, or advanced glycation end products (52, 61), suggesting that ponatinib-mediated ERK5 SUMOylation might be involved in ponatinib-associated atherosclerosis, VAEs and subsequent cardiovascular complications. Here, MAPK7 is linked to atherosclerosis.