In the unique cellular context of malignant B cells, MCC forms an interaction network centered at PARP1 and PHB2 to promote cellular survival and proliferation by up-regulating ERK activation, c-Myc, Mcl1, and cyclin B1, and by down-regulating p27 and suppressing cleavage of caspases 8 and 3. This evidence concerns the gene MYC and Merkel cell skin cancer.