While DTP3 has thus far produced no significant adverse effects in preclinical models or multiple myeloma patients, and unlike sensitive tumour cells, most normal cells do not constitutively express GADD45β, nor display spontaneous MKK7/JNK activation upon GADD45β inhibition, there remains a possibility that DTP3 administration will result in an exacerbation of MKK7/JNK signalling at sites of pre-existing inflammation, thus aggravating chronic inflammatory comorbidities and/or increasing the risk of autoimmune diseases. The gene discussed is GADD45B; the disease is AL amyloidosis.