In favor of the key role of CSB in UVB cytoprotection, as well as in the resistance to UVB‐induced senescence, dermal fibroblasts from a Cockayne syndrome patient with a mutation in the ERCC6 gene resulting in the loss of a functional CSB protein, but normally expressing the fusion protein were shown here to be dramatically more vulnerable to an acute high UVB irradiation dose and to form a much lower number of colonies after repetitive UVB exposure, compared to HDFs from normal donors. The gene discussed is ERCC6; the disease is Cockayne syndrome.