This extends previous studies in which Ask1 gene deletion or GS‐444217 treatment identified that ASK1 signalling is required for pathologic activation of p38 and, to a lesser degree, JNK pathways in the mouse obstructed kidney and in mouse diabetic nephropathy.23, 24 Thus, in three distinct models of renal injury induced by diverse insults (diabetes, mechanical stretch and immunity), it is possible that oxidative stress‐induced activation of ASK1 is a common mechanism for activation of p38/JNK signalling. This evidence concerns the gene MAP3K5 and diabetes mellitus.