MAP3K11 and persistent truncus arteriosus: Recently, MLK3 depletion by injecting an AAV-MLK3 vector (AAVMLK3−) into TAC-treated mice (TAC + AAVMLK3−) was found to significantly alleviate pressure-overload-induced cardiac dysfunction, fibrosis, pyroptosis, and ferroptosis more than control mice (TAC + AAVNC) [43,44].