Shajahan et al.44 reported that the phosphorylation of a tyrosine in caveolin-1 (Tyr-14) increased the sensitivity of breast cancer cells to paclitaxel, and the mechanisms that were involved in this process included the inhibition of BCL2 and BCL-xL by a c-Jun N-terminal kinase (JNK). The gene discussed is BCL2; the disease is breast carcinoma.