Summary UV‐B radiation inhibits plant growth, and this inhibition is, to a certain extent, regulated by miR396‐mediated repression of Growth Regulating Transcription factors (GRFs). Moreover, E2Fe transcription factor also modulates Arabidopsis leaf growth. Here, we provide evidence that, at UV‐B intensities that induce DNA damage, E2Fc participates in the inhibition of cell proliferation. We demonstrate that E2Fc‐deficient plants show a lower inhibition of leaf size under UV‐B conditions that damage DNA, decreased cell death after exposure and altered SOG1 and ATR expression. Interestingly, the previously reported participation of E2Fe in UV‐B responses, which is a transcriptional target of E2Fc, is independent and different from that described for E2Fc. Conversely, we here demonstrate that E2Fc has an epistatic role over the miR396 pathway under UV‐B conditions. Finally, we show that inhibition of cell proliferation by UV‐B is independent of the regulation of class II TCP transcription factors. Together, our results demonstrate that E2Fc is required for miR396 activity on cell proliferation under UV‐B, and that its role is independent of E2Fe, probably modulating DNA damage responses through the regulation of SOG1 and ATR transcript levels. Significance Statement At intensities that can induce DNA damage in Arabidopsis plants, E2Fc‐deficient plants show a lower inhibition of leaf size and an altered DNA damage response. The inhibition of plant growth by UV‐B mediated by E2Fc occurs epistatically over the microRNA396 and independently of E2Fe.