Autophagy-dependent changes in alternative splicing bias translation toward inflammation in senescent cells.

Despite limited translational capacity, senescent cells trigger inflammation by upregulating the translation and secretion of proinflammatory factors. In this issue of Developmental Cell, Kim et al. identify that altered autophagy and SFPQ-dependent EIF4H splicing during senescence redirects translation to promote inflammation, informing therapeutic strategies for cancer and other age-related diseases.